Interdisciplinary Studies (IDS)
Major in Neurobiological Sciences
The
IDS program is administered through the College of Liberal Arts and
Sciences
(Dean Sheila Dickison, 2014 Turlington Hall)
Visit
http://www.clas.ufl.edu/ids/
for application deadlines). The director for the
IDS
concentration in Neurobiological Sciences is
Dr.
Donald
Stehouwer (310 Psychology Bldg. ).
Applying
to
the Major
Get an application package from 2014 Turlington or download the application from http://www.clas.ufl.edu/ids/pdfs/IDS_app.pdf . In addition to personal information, a statement of purpose, and a current official transcript, you must include:
(1) a list of core courses for the major (minimum 20 hours 3000 level or above). These courses form the foundation of the major and are generally taken by all IDS Neurobiological Science majors. The 2000-level courses also constitute much of the pre-med curriculum, but they may not be used for the 20-hour core.
(2) a list of electives (minimum of 18 hours 3000 level or above). These are usually neurobiology-related courses and/or are relevant to your specific research project.
(4) a brief (~2 page) description of your research project, including hypotheses and experimental design, but not the detailed technical methods. Usually, this summary is written with help from your primary faculty sponsor.
(5) a letter of support from your primary faculty sponsor and from a secondary sponsor (see Information for IDS Sponsors). Your primary sponsor is the faculty member that will supervise your research project, and in whose laboratory you will conduct the research. The secondary sponsor serves as a consultant and is usually recommended by the primary sponsor. At least one of these two faculty must be a member of the College of Liberal Arts & Sciences. To find a primary sponsor, check the list at the end of this page or consult the list of faculty who are members of the McKnight Brain Institute at http://www.mbi.ufl.edu. and check the faculty directories of departments listed at the bottom of the page.
(6) a copy of your faculty sponsor's IACUC or IRB approval letter (not the entire protocol, just the approval letter) for this activity, if your work will involve live animals or humans.
(7)
signature of the Neurobiological Sciences program director, Dr. Donald
Stehouwer, 310
273-2168. Visit Dr. Stehouwer's web site at http://www.psych.ufl.edu/~steh
for
office hours.
(8) completion
of either PSB 3340 or PSB 3002.
Choosing
your
core and elective
courses
Chemistry,
through organic (CHM 3217 recommended) OR; Bio-organic (CHM
3218)
General
Biology (BSC 2010C AND BSC 2011C) with labs
General
Physics (PHY 2053 AND 2054, or higher)
Thesis
Writing for the Sciences (ENC 3254; recommended) Communicating in
Psychological
Science (PSY 3220)* OR Advanced Exposition (ENC 2210) OR
Technical Writing and Business Communication (ENC 3213)
Statistics (STA 2023 AND 3024)
Behavioral Neuroscience (PSB 3340; recommended) OR Introduction to Physiological Psychology (PSB 3004/PSB 3002 [same course, number has been changed])
Note
that the core curriculum above contains 12 credits at the 3000 level or
above. Therefore, to satisfy the core curriculum as outlined in
the
application, you should select three courses from the "track" core
courses below. The track listings are there to guide students
according
to their interests; you may select your core courses from any of the
three
tracks as part of your core.
*PSY
3220 has a Psychology lab course as a pre-requisite for
enrollment.
However, this pre-requisite is waived for IDS-NBS majors because their
laboratory requirement is satisfied by the senior thesis
research. To
enroll in this course, go to the Psychology Advisement Office (PSY Room
135)
and identify yourself as an IDS major. The advisor will then
over-ride
the pre-requisite and allow you to enroll.
Core course suggestions
reflecting different areas of concentration:
Cellular
and Molecular Neuroscience
Physiological Basis of Disease (PHA 5560C)
Intro to Biochem and Molecular Biology (BCH 5413)
Functional Human Neuroanatomy (GMS 6705)
Behavioral Neuroscience
Psychobiology of
Abnormal Behavior (PSB 4065)
Neurochemistry, Pharmacology and Behavior (PSB 4434)
Developmental Psychobiology (PSB 4504)
Chemical
Senses and Behavior (PSB 4654)
Neurobiology of Learning and Memory (PSB 4804)
Principles of Integrative Physiological Psychology(PSB
4823)
Cognitive
Neuroscience (PSB 4342)
Special Topics in Physiological Psychology (PSB 4934)
Comparative Psychology (CBH 3003)
Principles of Behavior Analysis (EAB 3002)
Applied Behavior Analysis (EAB 3764)
Cognitive Neuroscience
Psychobiology of
Abnormal Behavior
(PSB 4065)
Cognitive
Psychology
(EXP 3604)
Cognitive Neuroscience (PSB 4342)
Note: Your core must include at least 20 hours of credit in courses at the 3000 level or above.
Electives
You
elective choices should complement the focus of your research.
For
example, if you are studying genetic aspects of nervous system
function, a
course in genetics would be appropriate. Similarly, if your
research
focuses on clinical disorders, then a course in neuropsychology would
be
appropriate. The following lists of course electives are only
suggestions, and you may take other electives as appropriate.
Cellular &
Molecular
Neuroscience
Neurochemistry, Pharmacology and Behavior (PSB 4434)
Developmental Psychobiology (PSB 4504)
Genetics (PCB 3063)
Eukaryotic Cell Structure (PCB 3136)
Immunology (PCB 3255)
Animal Physiology (PCB 4745)
Embryology (ZOO 3605)
Comparative Histology (ZOO 4755)
Basic Biology of Microorganisms (MCB 3020)
Advanced Molecular and Cell Biology (BCH 6415)
Cell & Tissue Biology (BMS 5180)
Cell Differentiation, Morphogenesis and
Oncogenesis (BMS
5181)
Science, Myth and Value (PHI 2403)
Behavioral
Neuroscience
Additional
courses in
Behavioral Neuroscience (PSB 4XXX)
Comparative Psychology (CBH 3003) or
Principles of
Behavior Analysis (EAB 3002)
Sensory Processes (EXP 3104)
Functional Vertebrate Anatomy (ZOO 3713C)
Animal Behavior (ZOO 3513C)
Animal Physiology (PCB 4745)
Biochemistry
(BCH 4024)
Functional
Human Neuroanatomy (GMS 6705)
Genetics (PCB 3063)
Animal Physiology (PCB 4723C)
Cognitive
Neuroscience
Additional
courses in Behavioral Neuroscience (PSB 4XXX) or Cognitive
Science
(EXP 4XXX):
Sensory Processes (EXP 3104)
Finally, keep in mind
that the
IDS major is intended to be flexible, and that exceptions to both the
core and
the electives can be approved if the IDS committee agrees that they
better help
you to achieve your goals.
Research
Requirement
All IDS students must complete seven to twelve credit hours of research, which culminates in a senior thesis.
Information
for
IDS Sponsors
The
senior thesis research of IDS students should involve all phases of the
research enterprise, from experimental design, data collection, data
analyses
and data interpretation. The IDS student must submit a research
proposal that
not only outlines the broad research initiative, but which also
describes the
student’s role in that research.
The
letter from the primary sponsor should briefly identify the role of the
student
in the research, which should correspond to the student’s role as
outlined in
his/her research proposal. It should also include a statement that the
necessary physical, technical and intellectual support will be
available to the
student.
The
letter from the secondary sponsor should state that the sponsor has
reviewed
the student’s proposed curriculum and research project, and approves of
both.
Frequently
asked
questions
How
does an IDS major differ from regular majors?
IDS
majors may select an individualized set of courses that are usually
from
several different departments or disciplines.
IDS
students must perform a research project and submit and defend a senior
research thesis.
IDS
students must have a primary advisor (research mentor) and a secondary
advisor.
The two advisors must be from different departments (hence,
interdisciplinary) and one of them must be a member of the CLAS faculty.
When
should I apply to the IDS major, and what courses should I have already
taken?
Ideally, you should apply during your sophomore or junior years; if you wait too long, you may not be able to complete your schedule of coursework within the credit hour cap, and/or to complete a research project. Waiting until your senior year to change from a traditional major to the IDS major also undermines the argument that a traditional major does not satisfy your needs. There are no courses that you must have taken before applying, but completion of PSB 3004 or PSB 3340 is recommended prior to applying so that there is evidence of your interest in neurobiological sciences and that you will be successful in the major.
What
if I've been admitted to UF on an IDS track?
You must formally apply to the major the just as if you are changing from another major.
How
do I find a faculty sponsor?
Neurobiological
science is a very broad discipline, and studies range from those on
single
cells to those on neurological disorders. Some students already
identified a specialty of interest prior to applying to the major, but
many
have not. You should think about whether your primary
interests are
at a molecular level (e.g. study of single cells, genes, etc), at a
preclinical
but molar level (e.g. animal behavior, drug effects), or involves
humans either
in basic research (e.g. cognitive studies) or clinical issues (e.g. a
neurological disorder). Defining your general interests will help
you
narrow your search for faculty sponsors.
To find a primary sponsor, check the list below or consult the list of faculty who are members of the McKnight Brain Institute at http://www.mbi.ufl.edu. and check the faculty directories of departments listed at the bottom of the page. Select a few whose research sounds most interesting to you. Ask them (e-mail is the preferred way to make initial contact with faculty members) whether they are willing to mentor an IDS student and, if so, arrange a visit to their labs. Choose the mentor that's right for you in terms of research content and lab atmosphere. Remember, you will spend a lot of time in that lab, so be sure that you will be supported by the people there.
Can
I
get
credit for research that I have done before being accepted to the major?
Yes,
you can receive credit for research conducted under XXX 4905 in other
departments, but only if a letter grade is assigned for that
research. Research
credits
taken on an S-U basis may NOT be applied to the IDS research
requirement.
Research Mentors and their
Interests
Barry W Ache, Distinguished Professor, Director, Center
for Smell
and Taste
PhD, Physiology,
Primary
Department: Zoology, CLAS
Secondary Department: Neuroscience, COM
My research program, which is located at both the Whitney Laboratory
and the
McKnight Brain Institute, is directed at understanding the cellular
mechanisms
of chemosensory transduction, especially the interaction of the cyclic
nucleotide
and phosphoinositide signaling pathways and the functional implication
of
multiple signaling pathways on odor coding. My research uses both
marine
invertebrate and mammalian animal models. In addition, I also direct
the Center
for Smell and Taste, which fosters and integrates chemical senses
research and
training at the
bwa@whitney.ufl.edu
Kevin J
Anderson, Ph.D., Anatomy,
Primary
Department: Physiological
Sciences, CVM
Secondary Department: Neuroscience, COM
My lab is globally interested in the pathogenesis of hypoxic-ischemic encephalopathy in adults and the developing animals. Specifically we are exploring the relationship of several amino acid transporters and transport systems in the induction of hypoxic-ischemic brain injury. Moreover, we are intersted in the regulation of these systems following this type of injury. The systems under investigation include the excitatory amino acid transporters (EAATs) and several neutral amino acid transporters, including ASCT1 and SAT1/ATA1. All of these may contribute, in different ways, to the development of neuronal damage following an ischemic event through the efflux of intracellular stores of glutamate into the extracellular environment. This efflux of glutamate can lead to overstimulation of glutamate receptors and eventual cell death, a process termed excitotoxicity.
kanders@mbi.ufl.edu
Barbara-Anne Battelle, Ph.D., Biology,
Primary
Department: Whitney
Laboratory/Neuroscience, COM
Secondary Department: Biochemistry,
We study the modulation of retinal functions by signals from circadian clocks. We are particularly interested in understanding the biochemical mechanisms underlying the regulation of the photoresponse by circadian clocks. The effects of clock input on photoreceptors is being examined at several levels - gene expression, post-translational modification of proteins, and changes in structure. A current focus is to examine the function of a class III unconventional myosin that is found in photoreceptors of both vertebrates and invertrates. As with most unconventional myosins, the functions of this protein is unknown. It is, however, it a major clock-regulated phosphoprotein in some species and critical for photoreceptor function. We anticipate these studies will lead to a more complete understanding of photoreceptor function and of the causes of retinal degenerations.
battelle@whitney.ufl.edu
William Keith Berg, Ph.D., Psychology,
Primary
Department: Psychology, CLAS
My interests focus on uncovering the developmental changes in the brain-behavior relationships for executive functions including planning, response inhibition, and working memory. Methodologies to carry this out include cognitive behavioral studies, studies of brain electrical activity (EEG), and functional Magnetic Resonance Imagery (fMRI) with children, young adults, and older adults.
wkberg@ufl.edu
Stephen
J Blackband,
PhD Nottingham University,
Primary
Department:
Neuroscience, COM
Engaged in the development and application of
Magnetic
Resonance Imaging (MRI) and spectroscopy (MRS). Primary research
studies
include:-
1. development and application of MR microscopy. Primary applications
are to
single neural cell microimaging and studies of isolated perfused brain
slices.
The long term goal is to elucidate the origins of MR signals in
tissues.
Collaborating in the development of a web based MR mouse brain atlas.
2. development of high magnetic field MR techniques and technology.
This
includes novel volume and phased array radiofreqeuncy coil designs, and
their
application on our high field instrumentation.
3. development of diffusion tensor imaging and applications in animal
and human
studies.
blackie@mbi.ufl.edu
David
C Bloom,
Ph.D. Vanderbilt University, 1990
Primary
Department:
Molecular Genetics & Microbiology, COM
A major focus of my lab is the development of Herpes Simplex Virus (HSV) as a vector for expressing peptides in the nervous system. The natural neurotropism of HSV and its ability to be transported trans-synaptically make it a useful tool for studying the nervous system. Currently, our studies are focused in three main areas: 1) use of herpes vectors to express Fragile X Mental Retardation Protein (FMRP) in FMR1 knock-out mice to study the role of FMRP in Fragile X Disease, 2) testing a novel neurovirulence mutant of HSV for its efficacy in promoting regression of malignant glioblastoma in mouse and rat models, and 3) use of HSV as a neuroanatomic tracer to study the circuitry of the eye-blink reflex.
Donald C Bolser, PhD, Physiology, Univ of
Cough is the most common reason why sick patients visit physicians in this country. This reflex also is the most common manifestation of pulmonary disease. Ironically, relatively little is known about this important phenomenon. Over the last eight years my research efforts have focussed on identifying new drugs that inhibit cough by actions inside the central nervous system. Recent work has identified a common mode of action of a wide variety of centrally-acting antitussive drugs. The results suggest that centrally-active antitussive drugs inhibit cough at a common site of action. Results from these studies will expand our understanding of the mechanism(s) of action of antitussive drugs and the regulation of the central reflex pathway for cough. Studies in my laboratory are investigating the role of muscles of the upper chest, such as the pectoralis major, in the production of cough. These muscles are important because they stabilize the chest wall during cough. Furthermore, in patients with spinal injuries, upper chest muscles can be important in maintaining an effective cough reflex. For example, the pectoralis major muscle can compensate for loss of abdominal muscle function in spinally-injured patients and allow effective cough to be produced. We have found in animal models of cough that the pectoralis major muscle is controlled in a behavior-specific manner. That is, its pattern of activation can shift from inspiratory to expiratory during different respiratory defensive reflexes. This pattern of activation differs greatly from that of the diaphragm (the primary inspiratory muscle) and abdominal muscles (expiratory) which have stereotypical response patterns during inspiratory or expiratory respiratory defensive reflexes. Ultimately, these studies will lead to a greater understanding of the compensatory mechanisms that occur in pulmonary defensive reflexes following spinal injury..
bolserd@mail.vetmed.ufl.edu
David
R Borchelt,
PhD,
Primary
Department:
Neuroscience, COM
Over the past several years there has been tremendous progress in
identifying the genes that, when mutated, cause a number of
neurodegenerative
disorders, including familial Alzheimer\\\'s disease, familial
amyotrophic
lateral sclerosis, and Huntington\\\'s disease. These disorders are all
progressive, fatal disorders that result from the dysfunction and death
of
specific populations of nerve cells. In all of these disorders, a
change in the
amino acid sequence of specific proteins initiates a cascade of events
that
lead to disease. My laboratory has been committed to investigations
designed to
elucidate the molecular processes by which specific mutant proteins
cause
disease. This work involves the use of transgenic mouse models, in
which the
introduction of mutant human genes elicits a disorder that resembles
the human
disease, as well as cell culture systems to examine the effect of
mutations on
the function and biology of the mutated proteins. Collectively ,
these
approaches
provide insight into the molecular mechanisms of disease and
have
the potential to identify new therapeutic strategies for these
disorders.
Contact
information:
Margaret M
Bradley, Ph.D., Psychology,
University of Wisconsin-Madison,
Primary
Department: Psychology, CLAS
Secondary Department: Clinical & Health Psychology, CHP
Description of Neuro-related
Research:
Using different brain mapping techniques (e.g., functional magnetic
resonance imaging,
dense electrode EEG), we are investigating the neural mechanisms
underlying
affective and attentional processing in people with and without
diagnosable
anxiety disorders. Drawing on an animal model of motivation, we are
mapping the
subcortical and cortical neural circuits involved in emotional
perception and
imagery. In addition to neural mapping, we measure autonomic and
somatic
indices of affective and attentional mobilization, using
cardiovascular,
electrodermal, electromyographic and respiratory measures. Taken
together, our
research is consistent with the hypothesis that affective cues activate
basic
motivational circuits that have evolved to mediate appetitive and
defensive
behaviors.
bradley@ufl.edu
Marc N. Branch, Ph.D., Psychology,
Primary
Department: Psychology, CLAS
Primary research
interest in
how behavioral or experiential factors alter the way psychoactive drugs
change
behavior. Work is done with non-human primates and other non-human
animals.
Emphasis is primarily on behavior.
branch@ufl.edu
Adrie W
Bruijnzeel, PhD,
Neuropharmacology,
Primary
Department: Psychiatry, COM
My research focuses on investigating the neuronal substrates that
underlie acute
and protracted nicotine and opioid withdrawal. We attempt to reverse
the
affective signs of drug withdrawal by modulating neuropeptide levels in
the
entire brain, the central nucleus of the amygdala and the bed nucleus
of the
stria terminals We study the affective signs of nicotine withdrawal by
using
the intracranial self-stimulation (ICSS) procedure. This entails the
implantation of electrodes in the medial forebrain bundle of rats and
subsequently training the rats on the ICSS procedure. The acute
administration
of drugs of abuse lowers brain reward thresholds (i.e. potentiates
brain reward
function), while precipitated and spontaneous drug withdrawal results
in an
elevation of brain reward thresholds (i.e. deficit in brain reward
function).
In addition, we are investigating the long-term effects of exposure to
low
doses of nicotine and anesthetics in the air. We hypothesize that
chronic
repeated exposure to low doses of drugs of abuse induces adaptations in
brain
reward systems and brain stress systems which renders individuals more
sensitive for the development of a chemical dependency.
Corinna
Burger,
Ph.D., Neuroscience/Cell Develop, U.
Primary
Department:
Molecular Genetics and Microbiology, COM
I am interested in two main problems in molecular
neuroscience: the molecular biology of learning and memory in ageing,
and the
genetic mechanisms underlying neurodegenerative disorders. I have been
using a
differential gene expression approach to investigate the role of
putative genes
involved in central nervous system (CNS) function both in the normal
and
diseased states. I am using viral gene delivery to knock-down gene
expression
(by expressing ribozymes or small interfering RNAsm(siRNA)), or to
overexpress
normal or mutant forms of learning and memory candidate genes, in order
to
assign a role in behavior. The viral vector of choice is recombinant
Adeno-Associated Virus (rAAV). Here are some of gene discovery projects
in
which I am involved:
1. Differential Gene Expression Analysis of Learning and Memory
formation in
Aged Rats using Microarray Analysis - Human aging is associated with
cognitive
deficits, which are due in part, to impairment in the hippocampus. To
date,
only a few of the genes implicated in memory formation have been
identified, both
in normal and aging brain. I am trying to identify novel genes that are
involved in the memory impairment associated with aging by using the
powerful
Affymetrix microarray technology. In collaboration with Dr. Baker at
the
2. Gene Expression Profiles in Sprague-Dawley and Athymic Nude Rats
during
Acute, Subacute and Chronic Spinal Cord Injury - In collaboration with
Dr. Paul
Reier’s laboratory at the UF McKnight brain Institute, and Dr. Henry
Baker at
the Functional Genomics lab, we have carried out a time course study to
try to
elucidate the waves of gene expression that take place at different
times after
spinal cord injury. The goal is to find out new gene therapy approaches
for
spinal cord injury, using recombinant Adeno-Associated virus as a gene
delivery
vector.
3. The role of á-synuclein in Parkinson’s Disease (PD) - We are
attempting to
elucidate the function of á-synuclein in both normal brain function and
in PD.
Paul
R Carney,
MD,
Primary
Department:
Pediatrics, COM
Dr. Carney's primary focus of research is to develop an on-line, real-time Automated Seizure Warning and Prevention System for use by epileptic patients and their caregivers. His scientific work also involves genetic and neurophysiologic analysis of seizures in animal models and children. This program conducts bench-to-bedside research focusing on Brain Dynamics and Epilepsy. The Partnership brings together a multi-disciplinary group of research scientists who are pioneers in the areas of signal processing, optimization, hybrid VLSI and DSP, computation neurophysiology, neuroanatomy, epilepsy, and neurosurgery.
Brian Y Cooper, PhD, Biopsychology, Univ of
Primary
Department: Oral Surgery,
COD
Our laboratory examines the properties pain receptors or
nociceptors.
Nociceptors have evolved a variety of capacities to detect and
transduce mechanical,
thermal and chemical events. They also express paracrine agents that
they
release into tissue or into the synaptic cleft as co-transmitters. Our
laboratory has developed techniques that permit detailed examination of
the
discrete phenotypes of nociceptors and how they express different
combinationsof properties that reflect their tissue dependent
functional
specializations. Our focus has been mainly on heat, protons, ATP,
opioid,
eicosanoid and cholinergic mechanisms.
bcooper@dental.ufl.edu
Jesse Dallery, Ph.D., Associate
Professor
Primary department: Psychology
Choice, Substance Abuse, Impulsivity, Relapse, Cigarette Smoking
The goals of my research program are to connect basic behavior analysis
with
clinically relevant phenomena, and conduct studies within each
domain.
Using animal laboratory preparations, we’re examining some of the
fundamental
environmental variables and behavioral processes that regulate
behavior,
including drug abuse, impulsive behavior, and relapse. We use
quantitative models of choice as one lens through which to view and
understand
these complex phenomena. Some questions: How does chronic
nicotine
administration affect choice? What are some behavioral risk
factors that
increase the liability to drug effects? In a complementary
research
track, we’re applying the principles and processes studied in the
animal lab to
understand analogous behavior (drug abuse, cigarette smoking, impulsive
behavior, relapse) in humans. Cigarette smoking, the largest
preventable
factor leading to morbidity and mortality in developed countries, is an
important and practical target for inquiry and intervention.
We’re
developing several models to understand the dynamics of choice for
cigarettes,
including a behavioral model of impulsive choice. The laboratory
models
may be enormously useful for initial testing of both pharmacological
and
behavioral interventions designed for relapse prevention. Also,
these
models could further our understanding about whether and how critical
variables
(e.g., cue exposure, contextual factors, nicotine deprivation, drugs of
abuse,
pharmacotherapies, stress, etc) affect the impulsive choices that lead
to or
prevent relapse.
dallery@ufl.edu
Paul W. Davenport, Ph.D.,
Professor,
Primary
department:
Physiological Sciences:
Research in my laboratory combines invasive studies on animals with non-invasive human experiments to develop an understanding of the role of the cerebral cortex in respiratory sensations and the control of breathing. The transduction properties of respiratory muscle afferents are under investigation with the correlation of muscle mechanics with afferent discharge. The central projections of these afferents are studied electrophysiologically by recording thalamic and cortical neurons that are activated by respiratory muscle afferents. Cortical evoked potentials elicited by loads to breathing and psychophysical measures are used as a tool for studying respiratory sensation in humans. Respiratory load sensation is studied in adults, children and asthmatic patients. Psychophysical and evoked potential studies are being used with asthmatic patients that have difficulty sensing their asthmatic attack. The combination of the animal and human studies allows for identification of the neural mechanisms of respiratory load sensation and the related adjustments to breathing mediated by the cerebral cortex.
Trainee Participation in this Research: Students learn respiratory and neurophysiological methods including lung volume, airflow and pressure recording in humans and experimental animals for tracheostomy, arterial and venous cauterization, exposure of respiratory muscles, spinal laminectomy and craniotomy must be mastered. Electrophysiological techniques are used for recording single unit activity form peripheral nerves, dorsal rootlet recording, extracellular microelectrodes recordings in the central nervous system, brain surface electrode recording and muscle electromyography, In humans, skin electrodes are used for recording brain evoked potentials and muscle activity. Psychophysical methods are used in human studies of respiratory sensation. The physiological parameters recorded in these studies are processed by appropriate computer analysis.
DavenportP@mail.vetmed.ufl.edu
Thomas
B DeMarse,
PhD, Learning and Memory,
Primary
Department:
Biomedical Engineering, COEG
My research interfaces living rat cortical cells cultured in vitro to a computer to study neural computation, processing, and coding. Rat cortical neurons are cultured on a 60 channel multi-electrode array that can stimulate and record from neurons among a small population of about 25,000 cells. These neurons are interfaced to a robotic body via computer interface that acts as an artificial body. With this system we can manipulate many variables of interest (e.g., different patterns of sensory/stimulation inputs) and measure changes in the network's activity in real-time. Combined with optical imaging, this system represents a powerful platform to study how cortical neural networks process, learn and encode information.
Darragh
P Devine,
Ph.D., Psychology,
Primary
Department:
Psychology, CLAS
Research in my laboratory is currently focused on two major
projects. One project
deals with analysis of the physiological and behavioural consequences
of acute
and chronic stress exposure. We are currently examining the
neurobiology of
stress using highly emotional (as opposed to physiological) stressors,
as we
believe that this approach models the type of stress exposure that
humans
routinely experience. Human emotional stress exposure appears to be
very
important in the onset and maintenance of a variety of
psychopathological
conditions.
Accordingly we are examining individual differences in vulnerability to
stress-induced psychopathology, neuroadaptations that occur during
chronic
stress exposure, and the specific neurotransmitter systems and hormonal
systems
that participate in stress-induced psychopathology. We coordinate all
our
studies with examinations of behavioural concomitants of the stress
exposure,
and we focus largely on evaluation of anxiety-related behaviours.
The other major focus of my laboratory is the neurobiological basis of
self-injurious behaviour. Self-injury is a devastating behavioural
disturbance
that is expressed by individuals with autism, Lesch-Nyhan syndrome,
intellectual handicaps, and other conditions. The disorder is poorly
understood
at present. We have identified specific variables that confer increased
or
diminished vulnerability to self-injury, and we are examining the
neurobiological concomitants of this vulnerability to self-injure.
In each of these research endeavours, we combine a variety of
behavioural,
cellular and molecular analyses to uncover the neurological basis of
the
observed responses.
Fonda
Davis Eyler,
Ph.D., Developmental Psychology,
Primary
Department:
Pediatrics, COM
As a developmental psychologist my general area of research interest is the effect of perinatal variables on both the short and long-term developmental outcome of children who have experienced medical as well as psychosocial risks. More specifically I have been studying the developmental effects of prenatal cocaine exposure, separately and in interaction with other risk and protective factors experienced by children and their families. Currently, I am in my 11th year (of 15) of an NIH-NIDA sponsored prospective, longitudinal study of women and their children who were exposed to cocaine during pregnancy compared to a matched control group of the children of women who denied use and whose urine specimens were negative for cocaine or its metabolites on two unanticipated occasions. With a retention rate of >90%, we are now assessing the children's neurodevelopmental outcome, achievement, and behavior at 10 and 12 years old. The children and their primary caregivers are also being interviewed about their attitudes and behaviors including several psychosocial, family and home environment measures. The children's teachers and the school systems are also providing evaluations and data. In addition,we have received supplements to our RO1 that have been funding two minority researchers to collect or analyze data that complement our main study. An administrative supplement was also awarded to provide diffusion tensor and structural MRIs for a sub-set of our sample of cocaine exposed children and control subjects.
Roger
B Fillingim,
Ph.D., Psychology,
Primary
Department:
Operative Dentistry, COD
The major emphasis in our laboratory is human
psychophysical
research on sex differences in pain responses. We use a variety of
laboratory
pain procedures, such as cutaneous heat, pressure pain, ischemic pain
and cold
pressor pain. A large body of work now indicates that experimental pain
responses differ for women and men, with women typically exhibiting
lower
thresholds and tolerances and higher magnitude estimates of
suprathreshold
pain. In addition, we have demonstrated greater temporal summation of
thermal
pain among women. We have also reported on several biological and
psychosocial
factors that appear to influence experimental pain differently in women
and
men, including sex hormones, blood pressure, family history, pain
coping and
anxiety. We are also examining sex differences in responses to the
opioid
analgesics morphine and pentazocine. Several studies suggest that women
show
greater analgesic responses to “kappa-like” drugs, including
pentazocine,
nalbuphine and butorphanol. Recent work also indicates that morphine
may
produce greater analgesia in women. Interestingly, the rodent
literature generally
suggests the opposite. Thus, we are examining analgesic responses to
morphine
and pentazocine using three experimental pain models, and we are also
evaluating menstrual cycle effects on these responses.
Another interest in our laboratory is sex-related influences on
clinical pain.
In this regard, we have examined psychophysical responses in patients
with pain
conditions such as temporomandibular disorder (TMD), interstitial
cystitis, and
fibromyalgia, all of which are more prevalent in women than men.
A relatively new area of investigation involves ethnic differences in
pain
responses. We will be starting a new study of responses to multiple
experimental pain procedures in three different ethnic groups: African
Americans, Hispanic Americans and non-Hispanic whites. We will explore
perceptual, cardiovascular and neuroendocrine responses to pain in
these three
groups.
Ira
S Fischler,
PhD, Experimental Psychology,
Primary
Department:
Psychology, CLAS
have been using event-related brain potentials and EEG measures of neural activity to explore how anxiety and stress influence the comprehension of language that varies in emotionality. More generally, I am interested in the neural foundations of memory, and how this is modulated by affective variables.
Thomas
C Foster,
Ph.D.
Primary
Department:
Neuroscience, COM
My research has focused on understanding brain mechanisms for
modifying
synaptic transmission and their relationship to memory, particularly in
the
context of cognitive decline during aging. Synaptic plasticity is
thought to
mediate the associative and information storage properties of neurons,
and
intracellular calcium (Ca2+) levels occupy a pivotal position in
regulating
synaptic plasticity, determining whether synaptic strength increases or
decreases in response to neuronal activation. Interestingly, synaptic
plasticity processes change over the lifespan and thus could underlie
cognitive
changes with advanced age. Currently I am the principal investigator on
two
active grants that support work examining the mechanisms for memory
changes
during aging. Research funded by NIA characterized several biological
markers
of age-related memory impairment and provides a model linking
age-related
memory decline and a major hypothesis for aging, altered Ca2+
homeostasis, through
a change in Ca2+ signaling cascades to markers of brain aging including
the
shift in synaptic plasticity, increased susceptibility to neural
toxicity, and
altered gene regulation. Our current research is directed at examining
the role
of various sources of Ca2+ regulation in mediating age-related changes
and
testing the effectiveness of treatments in ameliorating memory decline
and
preventing/reversing markers of brain aging.
I am also funded through NIMH to study estrogen effects on hippocampal
function
across the lifespan. Interestingly, many of the effects of estrogen are
diametrically opposite to changes observed in aged memory impaired
animals. Our
work indicates that estrogen rapidly increases cell excitability and
the
strength of synaptic transmission. Importantly, our work suggests that
there is
a reduced responsiveness of estrogen signaling pathways with advanced
age. Our
future research in this area is directed at examining age-relate
changes in
estrogen signaling in the hippocampus at the behavioral, physiological,
biochemical, and genomic levels. As part of this work we employ
genetically
altered mice and we have initiated a number of studies using molecular
techniques (gene microarrys, RT-PCR, in situ hybridization)
In summary, my research program utilizes a combination of behavioral
characterization with biochemical, molecular, and electrophysiological
techniques to obtain a vertically integrated perspective on neural
aging, from
the molecular to the cognitive level.
Charles
J. Frazier,
Ph.D. University of Colorado, 1997
Primary
Department:
Pharmacodynamics, COP
Research in my laboratory is focused on identifying the specific
neurophysiological mechanisms through which cholinergic afferents
projecting
from the medial septum to the hippocampus contribute to the regulation
of
hippocampal excitability. At a cellular level, we study the functional
expression of both muscarinic and nicotinic acetylcholine receptors in
an
attempt to determine how activation and/or desensitization of these
receptors
can modulate the intrinsic behavior of hippocampal neurons. However, we
are
also interested in mechanisms through which activation of cholinergic
receptors
can modulate the behavior of both small groups of neurons (such as
interneuron
/ principal neuron pairs), and larger systems of neurons that are
capable of
generating coordinated activity.
This research is motivated by the fact that the septohippocampal
cholinergic
projection has been strongly linked to information processing and
memory
formation, as well as to highly characteristic patterns of neuronal
activity
such as gamma and theta rhythms. Degradation of this pathway has been
clearly
implicated in senile dementia and Alzheimer’s disease, and may play a
role in
other disorders that involve tight control of hippocampal excitability.
We approach these questions using in vitro preparations of rat brain
slices in
combination with differential interference contrast microscopy,
fluorescent
imaging, photometry, and multiple techniques of electrophysiology.
Jianbo
Gao,
Ph.D, Electrical Engineering, UCLA, 2000
Primary
Department:
Electrical & Computer Engineering, COM
Broadly interested in developing novel linear and
nonlinear Linda F.
Hayward, Asst
Professor,
BA, Psychobiology, Univ. of California at Santa Cruz, 1980
MS, Kinesiology, Univ. of Washington, 1984
PHD, Physiology, Northwestern Univ., 1990
Primary
Department:
Physiological Sciences, CVM
Four types of signals have been studied: EEG data for seizure
prediction/detection; fMRI data; Neuron firing data; Pathological
tremor data (including essential tremor and tremor in the
Parkinson's disease). Novel methods developed include chaos theory
based methods (recurrence time statistics; logarithmic displacement
curves, etc.) and random fractal theory based (mono- and multi-fractal).
Leslie
J Gonzalez Rothi,
PhD,
Primary
Department:
Neurology, COM
Dr Gonzalez Rothi has centered her research in two main arenas: (1) the cognitive neuropsychology of human communication as well as skilled, purposive, limb movement planning and performance, and (2) cortical plasticity in the mature CNS associated with new learning, functional recovery after CNS damage or injury, and response to rehabilitation. Currently she is funded by both NIDCD/NIH and the VA Rehabilitation Research and Development Service with clinical trials in treatment of aphasia, alexia, limb apraxia and aprosodia, the effects of adjunctive drug therapies in association with the previously listed treatment trials, and functional neuroimaging of functional recovery resulting from rehabilitation; health services research including the development of a brief cognitive inventory for use in prediction of treatment candidacy as well as functional outcome, development of a quality of life measure to be used in the context of aphasia after stroke; a large scale study of the interaction of language attributes in the context of aphasia, the impact of social factors such as race and marital status on outcome in aphasia, and the impact of intensity of treatment on outcome in aphasia.
Linda
F. Hayward,
PHD, Physiology, Northwestern Univ., 1990
Primary
Department:
Physiological Sciences, CVM
The primary focus of my research is to understand how central neural circuits interact to control blood pressure, heart rate and respiration. Currently my lab is investigating the role of specific regions in the pons (parabrachial nucleus) and midbrain (periaqueductal gray region) and the neurotransmitters important to these regions in descending control of sympathetic and parasympathetic drive in both the normal and the hypertensive animal. We utilize a combined approach of electrophysiology, neuroanatomy, immunohistochemistry and neuropharmacology to define the role of specific brain nuclei in autonomic control and to understand how this role changes in disease states. We are also interested in investigating the interaction between cardiovascular control and respriatory control and how specific nuclei and neurotransmitters modulate both systems either simultaneously or independently.
Jeffrey K. Harrison, Ph.D.
Primary department:
Pharmacology
Our laboratory is interested in the molecular characterization of G-protein coupled receptors. Collectively these receptors form a large superfamily of genes whose encoded proteins are characterized structurally as having seven stretches of hydrophobic amino acids that are capable of spanning the plasma membrane. Functionally, they mediate the actions of a wide variety of hormones, neurotransmitters, and drugs. Our research is focused primarily on receptors for chemokine (chemoattractant cytokine) peptides. We use a variety of experimental approaches with the goal to understand the location of expression and cellular signaling mechanisms of these receptors. Techniques in the lab include pharmacological, biochemical, immunological, and molecular biological methodologies.
Most of our attention is focused on determining the functional role of chemokines and their receptors in the central nervous system. Chemokines are a class of pro-inflammatory peptides that are important mediators of leukocyte migration. We have identified a number of chemokine receptors in the rat and have determined that the central nervous system expresses many of these genes. Chemokine receptors are being studied in transfected mammalian cells, primary cultured cells derived from rat brain (i.e. microglia, astrocytes, and neurons), as well as a number of neuroimmunological animal models.
harrison@pharmacology.ufl.edu
Marieta
B. Heaton,
Ph.D., NC
Primary
Department:
Neuroscience, COM
Our laboratory is investigating mechanisms underlying the fetal alcohol syndrome, a condition characterized by devastating central nervous system damage in children, following exposure to alcohol in utero. For these studies, we are examining neuroanatomical changes resulting from developmental alcohol exposure, and the molecular mechanisms underlying these changes. We hypothesis that one such mechanism contributing to developmental alcohol neurotoxicity is an alcohol-mediated alteration in the expression of vital neurotrophic factors (NTFs) and/or their receptors. Alcohol also has well-defined effects on the cellular redox state, enhancing generation of destructive reactive oxygen species (ROS) and decreasing expression or activities of endogenous antioxidants. We therefore further hypothesize that alterations in NTF availability impact significantly on the cellular capacity to accommodate alcohol-induced ROS, since NTFs normally regulate the cellular redox state, by enhancing expression of antioxidants, and inhibiting ROS production, while increased ROS per se can lead to reductions in NTF expression through downregulation of NTF transcription. We propose that an additional mechanism critical to developmental alcohol neurotoxicity is the modulation of expression of cell death and survival genes. Experiments underway are investigating intracellular events, such as alcohol-mediated alterations in NTF signal transduction, which may underlie alcohol influences on each of these interacting processes. We are further investigating the possibility of amelioration of these destructive ethanol effects by application of exogenous antioxidants. Techniques being used include quantitative neuroanatomical analyses, immunohistochemistry, primary neuronal cell culture, neuronal survival assays, reactive oxygen species and antioxidant assays, and Western blot and ELISA protein quantification. These studies have the potential to elucidate important inter-related intracellular mechanisms underlying the devastating CNS damage seen in the fetal alcohol syndrome, and may suggest possible therapeutic strategies for ameliorating this damage
Linda Hermer-Vazquez, Ph.D. Biological Psychology and
zCognitive
Studies,
Primary department: Psychology (CLAS)
Most of my research focuses on the complex neural circuit dynamics
underlying
decision-making and working memory. Our laboratory uses rats for
these
studies because it has been shown that in the olfactory domain, rats
exhibit
decision-making and other sophisticated abilities on a par with
primates (which
are usually tested in the visual domain). For these studies, we
implant
bundles or arrays of microelectrodes in the rat olfactory cortex, in
choice-making areas of the prefrontal cortex, and the motor cortex, and
simultaneously record action potentials and local field potentials
(LFPs)
simultaneously as rats learn and execute these tasks. In another,
newer
project, I am studying how primary motor and prefrontal circuits
"offload" the neural processing underlying cognitive and motor skills
to the cerebellum and rubrospinal pathway once the tasks are well
learned, or
"automated." Finally, I am part of a project that involves
using grid computing to model how motor cortical neurons encode
"volitional" motor commands so that a paralyzed patient can control a
robotic device with his "thoughts," bypassing the injured spinal
cord. I especially encourage students with a strong interest in
neuroscience and engineering to apply.
Dena R. Howland, Ph.D.
Primary Department: Neuroscience:
The overall focus of the laboratory is to determine how the spinal
cord
responds to injury and what interventions may be used to enhance
recovery based
upon both anatomical and behavioral criteria. A variety of lesion
models
in both the rat and cat are being used. Our studies have shown
that
grafts of embryonic spinal cord can promote recovery following spinal
cord
injury in both developing and adult systems. These grafts can survive
for long
periods and undergo substantial differentiation. Although grafts
into
adult and developing systems both integrate with the host tissue, the
grafts
integrate more extensively and promote greater axonal growth when
placed into
the developing host system. This structural response difference
is
correlated with differences in behavioral recovery. We are
continuing to
assess the potential for grafts of embryonic spinal cord to enhance
behavioral
recovery and promote anatomical repair in the adult and believe that
the
mechanisms by which transplants may work in the adult versus developing
system
are different. A variety of neuroanatomical and molecular methods
are
being used to assess the cellular and axonal interactions that occur
between
the host and graft. The behavioral analysis focuses on several
characteristics
of locomotion including weight support, balance, interlimb coordination
and
angular kinematics. We are also currently studying the expression
of
several molecules that are know to affect axonal growth during
development. These molecules include both growth-promoting and
repulsive
molecules as well as their putative receptors (e.g. netrin,
proteoglycans,
aggrecan, dcc). The differential display of these molecules in
the adult
and following injury may suggest mechanisms that affect growth which
are present
or absent in the developing versus adult versus injured systems.
These
differences may also suggest potential therapeutic strategies for the
adult. To this end, we are degrading proteins as well as
introducing
genes to make proteins within the injured central nervous system.
In
addition to repair strategies using cellular and molecular approaches,
we are
also evaluating the effects of rehabilitation training paradigms on
recovery in
experimental animal models. These studies should begin to
indicate
whether training is important, whether the type of training is critical
and
whether training can be beneficial,
detrimental or benign based upon behavioral and anatomical criteria.
Richard
D Johnson,
PhD,
Primary
Department:
Physiological Sciences, CVM
- In vivo and in vitro
electrophysiology, neuroanatomy, and immunohistochemistry of the single
sensory neurons, spinal cord and brainstem interneurons, and
motoneurons mediating control of the reproductive and pelvic visceral
organs; normal mechanisms, role in reproductive behavior and
micturition, sensory and motor dysfunction following chronic spinal
cord injury, chronic pain, efficacy of neural transplantation in
recovery of function.
Electrophysiology, neuroanatomy, and immunohistochemistry of the peripheral nerves with respect to chronic nerve injury and nerve regeneration; response properties of primary afferent receptors in skin, viscera, muscle, and efficacy of target-specific nerve trophic factors in recovery of function
David Julian, Ph.D., Univ
Primary department: Zoology, CLAS
The focus of my laboratory is on ecological and comparative physiology. We are currently investigating the cellular and molecular adaptations of marine and aquatic invertebrates to hypoxia and hydrogen sulfide. Both hypoxia and sulfide commonly occur in many marine environments, including hydrothermalvents, mudflats, mangrove swamps and salt marshes. Sulfide is also a byproduct of some industrial processes, and although many humans are regularly exposed to this toxin, its long-term neurological effects are very poorly understood. Therefore, the objectives of our research are twofold: first, we hope to understand how some marine invertebrates can tolerate, and even thrive, in extreme and seemingly toxic conditions, and second, we hope to clarify the cellular and molecular mechanisms by which humans and other vertebrates are affected by these same challenges. In this research, we use a variety of animal and in vitro models, including marine worms, aquatic fish, the nematode C. elegans, and mammalian neuronal and glial cell cultures. The interdisciplinary nature of this research allows us to take advantage of the power and flexibility of modern molecular biology and neurobiology techniques, which up to now have been little used for studies of marine and aquatic invertebrates.
Michael
J Katovich,
PhD, Physiology,
Primary
Department:
Pharmacodynamics, COP
My lab focuses on six main research areas, which include: alterations in the renin-angiotensin system in hypertension and diabetes, temperature regulation, vascular reactivity, menopause,opiate dependency, and thirst. To study these areas, we utilize a combination of gene therapy approaches and classical physiological methods.
Maureen
Keller-Wood,
Ph.D., Univ.
Primary
Department:
Pharmacodynamics, COP
My overall research interest is the physiologic adaptations to
pregnancy.
The laboratory is focusing on changes related to cortisol effects at
the two
receptors at which adrenal steroids (such as cortisol) bind: the
mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR).
These
receptors mediate physiologic effects necessary for regulating blood
glucose,
blood pressure, fluid and electrolyte excretion, appetite, and mood. In
the
brain and pituitary, these receptors are also critical for the proper
regulation of adrenal secretion through feedback effects. In
particular, we are
interested in the role of these receptors in two inter-related
adaptations of
pregnancy: changes in regulation of the blood pressure and fluid
balance, and
the changes in feedback control of the hypothalamo-pituitary-adrenal
(HPA) axis
which allow a chronic increase in ACTH and cortisol levels during
pregnancy.
One of these projects has a major neuroscience component. In this
project we
are testing the hypothesis that during pregnancy progesterone
antagonizes
cortisol action at mineralocorticoid receptors (MR) in the hippocampus,
which
in turn reduces the feedback effect of cortisol and allows ACTH (and
therefore
cortisol) to chronically increase. We are looking at both physiologic
changes
in HPA function, changes in MR and GR pharmacology, and changes in
corticosteroid-regulated genes and proteins in hippocampus, such as
serotonin
receptors. The model systems we use are pregnant and
progesterone-treated ewes,
and hippocampal cell cultures.
We are also beginning a study to examine the ontogeny of MR and GR
expression
and action in the late gestation fetus. Although GR-related actions are
known
to be crucial for normal lung and GI development at the time of birth,
we are
interested in whether MR-mediated actions precede this and cause
induction of
genes important for maturation in the fetus. Among the sites we are
interested
in studying are the brainstem and the hippocampus. It is known that
estrogen
and progesterone exert developmental effects on neurons, in particular
hippocampal neurons, and may also help “mature” pathways important for
responses to cardiovascular “stress.” In these experiments we will look
at the
ontogeny of MR and GR in brainstem and hippocampus, as well as the
induction of
putative MR-induced genes, such as sgk and sodium channels.
Jeffrey
A.
Kleim, Ph.D.
Primary
department:
Neuroscience
(COM)
-- and VA Medical center
The brain is a highly dynamic organ that is capable of structural and functional reorganization in response to a variety of manipulations. This neural plasticity is the mechanism by which the brain encodes experience. My laboratory examines how plasticity within rat and human motor cortex supports learning in the intact brain and “relearning” after stroke. We use intracortical microstimulation in rats and transcranial magnetic stimulation in humans to examine how motor training alters the functional organization of motor cortex. This work has demonstrated that rehabilitation-dependent recovery of motor function after stroke is associated with a reorganization of movement representations in rodent motor cortex. Furthermore, there are specific behavioral and neural signals that drive both recovery and plasticity. These experiments are being used to test novel therapies for enhancing motor recovery in stroke patients.
Eric
D Laywell,
Ph.D., Anatomy & Neurobiology,
Primary
Department:
Neuroscience, COM
My research aims are:
1) identification and cultivation of multipotent neural stem/progenitor
cells
from a variety of brain tissues;
2) transplantation of stem/progenitor cell to test engraftability and
integration within both normal and injured brain areas;
3) exploration of the potential for transdifferentiation of non-neural
stem
cells (i.e. hematopoietic and hepatic); and
4) analysis of subventricular zone anatomy and cytoarchitecture.
Mark H. Lewis, Ph.D., Ph.D.,
Primary
Department:
Psychiatry, COM
The research interests of this lab involve clinical and animal model studies of autism and related neurodevelopmental disorders. Specifically we are focused on the abnormal repetitive behavior (e.g., stereotyped behavior, compulsions, rituals, insistence on sameness) characteristic of children and adults with autism and related neurodevelopmental disorders. In our clinical studies, we are examining how restricted, repetitive behaviors in autism are related to deficits in motor control (control of involuntary and voluntary movements), and cognitive flexibility (behavioral inhibition, set shifting, exploration). In our animal studies, we are investigating the neurobiology underlying the development and expression of abnormal repetitive behavior in a mouse model. One research direction involves examining the brain changes associated with the prevention of abnormal repetitive behavior by early experience. Other work in the lab is focused on using pharmacological and biochemical methods to identify the neural circuitry mediating abnormal repetitive behavior in these animals.
Trainees working on projects related to our animal model will be able to learn a variety of techniques relevant to the neurobiological basis of behavior. These include, but are not limited to, stereotaxic surgical techniques, automated and observational behavioral assessment, pharmacological methods, and biochemical methods (e.g., immunoassay and histochemical techniques) to examine brain changes.
Yijun
Liu,
PhD,
Primary
Department:
Psychiatry, COM
The research interest in this lab, located at the
Current work includes:
(1) Using fMRI to probe the neuropathological and neuropharmacological
bases of
certain psychiatric disorders, such as affective disorders (e.g.,
Obsessive-Compulsive Disorder), Autism/Abnormal Repetitive Behavior,
Schizophrenia, etc., and their treatment;
(2) Development of in vivo neural-system modeling methods to explore
the role
of subcortical structures (e.g., the thalamus, basal ganglia, midbrain,
and
cerebellum) in the perceptual and adaptive processes underlying human
cognition
and affection, and especially, in the maintenance of our (self-)
consciousness;
(3) Developemnt of approaches to the real timing of neural-hormonal
interaction, e.g., an fMRI model of hypothalamic function in the
control of
feeding behavior and use these approaches to study obesity, diabetes,
drinking
and gambling problems, and eating disorders (inclduing substance abuse)
in
humans; and
(4) A Dynamic Brain Mapping (DBM) program using the real-time fMRI
techniques,
with integration of recent development in MR phase imaging, perfusion
imaging,
and diffusion imaging.
yijunliu@ufl.edu
Ron
Mandel,
Ph.D,
Primary
Department:
Neuroscience, COM
Gene transfer for the study of neurodegenerative disorders such as
Parkinson's disease, Huntington's disease, Canavan disease, Leigh
syndrome, and
stroke.
Trainees are welcome to participate in all phases of the laboratory which include stereotaxic surgery, behavioral testing, histology, immunocytochemistry, and some molecular techniques.
Thomas
H Mareci,
Ph.D.,
Primary Department: Biochemisty and Molecular Biology, COM
Our research program uses nuclear magnetic resonance (NMR)
techniques to
study fundamental questions of tissue structure and biochemical
processes in
living systems. We examine excised tissue with MR microscopy and
spectroscopy;
extending these measurements to studies in vivo. We develop unique NMR
measurement and processing methods, and custom hardware/software
systems for
our studies of cellular and molecular processes. Our current projects
are the
following:
1) Study blood-spinal-cord barrier and blood-brain barrier disruption,
using
dynamic contrast enhanced MR imaging in vivo, following trauma. As part
of this
study, we are modeling the kinetics of lesion enhancement in a
longitudinal
study of barrier disruption over weeks;
2) Use diffusion tensor imaging to map fiber tracts in highly
structured white
matter and gray matter of nervous tissue. Using this method, we are
mapping the
fiber structure of the brain and spinal cord following trauma;
3) Design unique RF coils for implantation to enhancement sensitivity.
These
implanted coils are inductively coupled to an external coil during
measurements
and provide a gain up to a factor of 4 in signal-to-noise ratio.
Because of the
gains possible, these coils allow the acquisition of very high spatial
resolution MR images and spectra.
Michael
Marsiske,
Ph.D.,
Primary
Department:
Clinical and Health Psychology, CHP
older
adults'
everyday
problem solving abilities, their relationship to basic
cognitive and
intellectual performance and to functional competence, and the role of
social
partners in cognitive collaboration
(2) the range of modifiability (plasticity) in adults' intellectual
functioning, with a particular recent focus on intraindividual
variability and
inconsistency in elders' cognitive performance, and
(3) antecedents (especially sensorimotor) of individual differences in
adult
cognitive and intellectual functioning. Much of this research focuses
on the
interdependency of postural control (balance) and complex cognition in
later
life
Ed
Meyer,
PhD, MIT, 1978
Primary
Department:
Pharmacology, COM
My research group develop models for age-related neuropathological
disorders
and novel treatment approaches for these disorders as well.Some models
and
treatments are based on somatic gene transfer, others on more classical
anatomical,
cellular, and pharmacological approaches. Work in the lab extends from
molecular biology and virology (generating new AAV derived vector
systems for
gene transfer into brain) through behavior, with a significant amount
of cell
biology (including a new project with embryonic stem cells)thrown in.
Drake
Morgan, PhD,
UNC
Primary
Department:
Psychiatry, COM
There are several lines of research being
investigated in
Dr. Morgan’s laboratory. We are still developing models of addiction in
rats
and trying to identify predictors and consequences of this behavior.
Behavioral
studies include drug self-administration, drug discrimination,
schedule-controlled behavior, “impulsivity” and other operant testing,
and
locomotor activity. There is a continuing interest in opioids and
cocaine,
which may branch off towards other drugs of abuse, including MDMA,
methamphetamine, nicotine, THC, and alcohol. Additional areas of
research
include the examination of changes in the sensitivity to pain and
opioids as a
function of aging.
David F
Muir,
Ph.D., City Univ of NY,
My research examines peripheral nerve and spinal cord regeneration
with the
intent to develop therapies for improved functional recovery after
traumatic injury.
A second effort investigates peripheral nerve sheath tumors and
mechanisms of
tumorigenesis.
Our work in neuronal regeneration has focused on two main issues:
1) discovering the fundamental mechanisms by which nervous system
regeneration
is regulated and
2) developing technologies to remove inhibitors of nervous system
regeneration
to improve recovery of function after injury. Our inceptive studies in
peripheral nerve injury models show that neuronal regeneration can be
inhibited
by a class of extracellular molecules called chondroitin sulfate
proteoglycans
(CSPG). We discovered that peripheral nerve injury induces the
expression of
extracellular matrix-degrading enzymes that degrade and inactivate
inhibitory
CSPG. Our work indicates that CSPG-degrading enzymes can markedly
improve the
regeneration of transected nerve in animal models and suggests a low
risk
adjunctive therapy to improve the outcome of conventional nerve repair
surgery.
This approach has also been applied to a major clinical challenge to
enable the
use of allogenic and xenogenic nerve grafts in the large number of
patients
with intractable nerve deficits. Related work in a spinal cord injury
model
gave promising evidence that inactivation of CSPG by enzymatic
degradation can
improve the growth promoting potential of the spinal cord as well.
Investigating the therapeutic value of enzymes that degrade inhibitory
CSPG
have a great potential to overcome our present inability to prevent
functional
loss resulting from nervous system injury.
My research in peripheral nerve sheath tumors centers on tumorigenesis
in
Neurofibromatosis type 1 (NF1). NF1 is a common autosomal dominant
disease
characterized by a high incidence of neurofibroma. My collaborative
studies
test the hypothesis that the Schwann cell is initially mutated and
clonally
expanded in neurofibromas. We have established numerous Schwann cell
lines from
neurofibromas and have documented numerous genetic alterations in these
cells.
We recently developed a working xenograft model for plexiform
neurofibroma in
mice with an NF1 background. Present aims focus on the mechanisms
underlying
neovascularization and vascular requirements in neurofibromas with the
goal of
testing the response of neurofibromas to anti-angiogenic therapies.
Harry
S Nick,
PhD,
Primary
Department:
Neuroscience, COM
Our laboratory is interested in understanding the molecular
mechanisms
which control tissue specific gene regulation. Research has focused on
proteins
which exhibit both pro- and anti-inflammatory activities in the lung,
intestine
and brain. These genes include manganese superoxide dismutase (MnSOD),
a potent
cyto protective anti-oxidant protein, the inducible nitric oxide
synthase
(iNOS) gene which generates elevated levels of the powerful
neurotransmitter
and vasodilator, nitric oxide (NO) and cytoplasmic phospholipase A2
(cPLA2)
which controls intracellular levels of arachidonate metabolites. These
genes
are also linked through transcriptional regulation by a subset of
pro-inflammatory mediators, including bacterial endotoxin (LPS),
interleukin 1
(IL-1), tumor necrosis factor (TNF-a) and interferon-g.
Sara Jo Nixon
Primary department: Psychiatry, COM
The research interests of my lab focus on the neurocognitive consequences of severe drug abuse in humans, focusing on alcohol but including polydrug and other aspects.
Lucia
Notterpek,
PhD,
Primary
Department:
Neuroscience, COM
The overall interests of the laboratory are the cellular
interactions of
neurons and glia during the development of the nervous system and how
these
processes are altered in disease. A key element for neuronal
functioning is
myelination, the glial ensheathment of axonal processes that serves to
facilitate signal propagation from the neuronal cell body to the
synaptic
terminal. A glial molecule termed peripheral myelin protein 22 (PMP22)
has been
shown to have key roles in normal nerve development, since point
mutations,
deletions or duplications of the PMP22 gene are associated with nerve
degeneration and disease. It is the main goal of my laboratory to
define the
roles of PMP22 in the peripheral nervous system and in the pathogenesis
of
neuromuscular disorders.
A major area of research is to elucidate how altered turnover rate and
intracellular
trafficking of mutated PMP22 contribute to the progressive subcellular
pathogenesis of PMP22-associated demyelinating neuropathies. Recent
data
suggest that inhibition of the ubiquitin-proteasome pathway in Schwann
cells
leads to accumulation of the endogenous PMP22 in newly-defined
ubiquitin-containing cytoplasmic inclusions, called aggresomes.
Aggresomes are
thought to form when proteasome activity gets saturated due to the
expression
of misfolded proteins. Furthermore, both overexpressed wild type and
mutated
PMP22s also aggregate in pericentriolar aggresomes. Three specific
questions
that arose from these findings are currently being addressed
1) What is the role of the ubiquitin-proteasome pathway in the
pathogenesis of
peripheral neuropathies?
2) What are the effects of aggresomes on Schwann cell biology?
3) How does overexpression of, or point mutations in, the PMP22 gene
affect the
turnover rate of PMP22 (and of other myelin proteins) and in turn
myelin
stability?
Another major area of investigation is to define the role of PMP22 in
Schwann
cell biology. Studies indicate that PMP22 is a component of
intercellular
junctions in epithelial and endothelial cells, and shares significant
homology
with the claudin tight junction proteins. Utilizing molecular and
biochemical
tools, we are investigating whether PMP22 is a functional or structural
component of intercellular junctions, first in epithelial and
endothelial cells
and then in myelinating Schwann cells. A goal of these studies is to
establish
a functional assay where we can evaluate the roles of PMP22 in normal
cells and
in the disease paradigms.
Roger
L Papke,
Ph.D. Cornell University, 1987.
Primary
Department:
Pharmacology and Therapeutics, COM
We study neuronal nicotinic acetylcholine receptors (nAChR) in order
to
understand the role that these receptors play in the basic function of
the
brain. While the nerve cells of the brain are very complex, activated
or
inhibited by many different kinds of drugs, with specific drugs perhaps
even
having more than one kind of effect on a single cell, there are ways to
study
these nicotinic receptors that makes it easier to understand how
nicotine and
related drugs may be working in the brain. One way we do this is to
utilize the
genes for these nAChR which have been isolated and cloned. We make
copies of
the genes, in the form of RNA, to be injected into Frog oocytes. After
a few
days the oocytes can be stimulated by nicotinic drugs, the same way
that a cell
in the brain might be. Another approach we take is to study the natural
occurring brain nicotine receptors, either in acutely dissociated
neurons, or
by recording from neurons in brain slices. By studying the neurons in
brain
slices we can determine how nicotinic drugs affect connections between
cells,
and also how treatments to the whole animal can affect circuits within
the
brain.
We study drugs that either act like nicotine, or alternatively may
block the
effects of nicotine, either in vitro (with oocytes) or ex vivo (in
brain
slices). In this way we hope to learn the different effects these drugs
may
have in specific parts of the brain, including those known to be
involved with
learning and memory (e.g. the hippocampus) addictive behavior, or other
brain
function related to brain nAChR.
A second major goal in the lab is to use the nAChR as general models
for
synaptic receptors of the type which directly couple drug binding to
the
generation of electrical currents. We are identifing parts of the
molecule
which are important in coupling the binding of neurotransmitters to the
conformational change associated with the active form of the receptor.
We study the roles that various parts of the receptor protein play in
determining how the receptor functions by using recombinant DNA
techniques to
create new forms of the genes (mutants and chimeras) that will combine
or
exchange the properties of the different forms of the receptors. We
study both
the pharmacology and the biophysics of these artificial receptors. Some
of the
experiments make use of patch-clamp techniques to study the currents
that flow
through single molecules when they are activated by nicotine or other
drugs.
Panos
M Pardalos,
PhD,
Primary
Department:
Industrial and Systems Engineering, COEG
Epilepsy is among the most common disorders of the
nervous
system (second only to stroke).
For the vast majority of patients, epileptic seizures occur in the
absence of
identifiable
external precipitants. Thus, one needs to look into the characteristics
of the
epileptogenic brain itself to find an explanation for the intermittent
occurrence of epileptic
seizures. Given the complexity of brain circuitry and recent results,
it is
highly likely that the brain behaves in a nonlinear fashion. If this is
the
case,
the dynamical features of the epileptic brain (especially the
transition to
epileptic
seizures) may be explained by the theory of nonlinear chaotic systems.
Measures
derived
from the theory of nonlinear dynamics and discrete optimization
techniques are
used
for prediction of impending epileptic seizures from analysis of
multielectrode
electroencephalographic (EEG) data.
Joanna Peris, PhD,
Primary
Department:
Pharmacodynamics, COP
The primary interest of my lab is understanding
the
neurochemical mechanisms of ethanol addiction. As part of this
research, we
measure how dopaminergic and amino acid neurotransmission in brain
regions highly
implicated in the alcohol addiction process (e.g., nucleus accumbens)
are
altered in rats exhibiting high degrees of ethanol self-administration.
The
combination of on-line capillary electrophoresis separation and
laser-induced
fluorescence detection with in vivo microdialysis in awake behaving
animals
provides a remarkable insight into the details and mechanisms of
ethanol-induced changes in neurotransmission. In particular, the
ability to
measure second-to-second fluctuations in dopamine, taurine and other
amino
acids during periods of ethanol craving and subsequent
self-administration will
be important in helping delineate the neurochemical mechanisms
underlying the
addictive process vs that underlying actual alcohol intoxication.
We induce rats to willingly and reliably self-administer ethanol
without food
or liquid deprivation.and then implant cannula into the relevant brain
regions
of the animals. So far, we have revealed some very novel findings about
the
time course of changes in taurine and dopamine in the first few minutes
after
both ethanol injections and self-administered ethanol in naïve and
alcoholic
rats. Related studies include determining the changes in both
excitatory and
inhibitory transmission that take place in hippocampus after chronic
ethanol
exposure that may account for decreases in long-term potentiation and
memory
decrements caused by such treatment.
Steven
M. Phelps, Ph.D.,
Univ of
Primary
Department: Zoology,
CLAS
We
are interested in the mechanisms of animal behavior and how those
mechanisms
evolve. The lab employs a diverse array of approaches, ranging from
computational models to the molecular analysis of gene expression. This
work is
strongly anchored in empirical studies of animal behavior in both the
laboratory and field. Current projects are aimed at understanding the
role of
the vasopressin V1a receptor in rodent social behaviors. We would like
to know
why the vasopressin receptor shows so much within and between species
variation
in brain expression, and how this variation in neural phenotype
contributes to
social behaviors. The behaviors we study include the formation of
pair-bonds in
the monogamous prairie vole, and the production and perception of
advertisement
calls in the singing mouse. These projects involve substantial field
components
in both the
Mohan
K Raizada,
Ph.D., 1972, Biomedical Science,
Primary
Department:
Physiology and Functional Genomics, COM
Project I
We have established that the brain Renin-Angiotensin System (RAS) is
the key in
the control of blood pressure (BP) and its dysregulation results in
hypertension. Our laboratory has been involved in elucidating
mechanisms of
this dysregulation in order to develop novel therapeutic strategy for
central
control of hypertension. The following lines of investigations are
underway: A:
Elucidation of signal transduction mechanisms of Ang II-induced
Norepinephrine
(NE) neuromodulation in neurons. The role of various signaling kinases
on Ang
II-induced vesicular trafficking, NE release, and synthesis are being
investigated. B: Mechanisms of an hyperactive neuronal AT1 Receptor in
the
spontaneously hypertensive rat (SHR) is being investigated. We are
testing a
hypothesis that this hyperactivity is a result of a novel coupling of
the AT1
receptor to a unique signaling system in the SHR neurons. C: Expression
profiling is being used to identify known and unknown genes that are
regulated
by Ang II in order to discover hypertension-linked genes in the brain.
Project II
Our previous studies have established that a single intracardiac
injection of a
retroviral vector containing either AT1 receptor antisense cDNA or
ACE-antisense cDNA prevents animals from developing hypertension for
life. This
is an exciting observation and provides conceptual support that
antisense
targeting of the RAS is an important strategy for the long-term control
of
hypertension. The following lines of investigation are underway in this
area:
A: Provides further conceptual support for antisense gene therapy by
using many
different models of hypertension. B: Use lentiviral-based vectors to
determine
a long-term reversal of hypertension. C: Explore the possibility of
using
tissue/cell specific promoters to drive the expression of antisense and
determining the role of tissue RAS in hypertension. D: Develop a
tet-regulated
AT1R-AS expression system for in vivo use. Our objective is to turn on
and turn
off the expression of AT1R-AS in vivo on demand and study its effects
on
hypertension. E: The cardiovascular-protective role of the AT2 receptor
and ACE
2 is being investigated. We are testing the hypothesis that
overexpression of
this receptor and novel enzyme (ACE 2) may protect animals from
hypertension.
Roger
L Reep PhD,
Primary
Department:
Physiological Sciences, CVM
My research is focused in two main areas:
development of a
rodent model for studying the neglect syndrome, and manatee
neurobiology.
Neglect is a human neurological disorder characterized by a failure to
report,
respond, or orient to novel or meaningful stimuli presented to the side
of the
body opposite a brain lesion, and is not explainable by a primary
sensory or
motor deficit. Some manifestation of neglect is found in about 40% of
all cases
of right hemisphere brain damage, typically produced by stroke. Neglect
most
often involves damage to a neural network for directed attention which
includes
specific regions of the cerebral cortex, thalamus and striatum. This
disorder
is disabling to patients and their families and is extremely difficult
to treat
because neglect patients are often not concerned with or aware of their
neurological status. There are no effective therapies for neglect, and
if
recovery occurs it is usually incomplete. Over the past 20 years, we
and others
have developed a rat cortical model of neglect which demonstrates
direct
behavioral, anatomical, and pharmacological applicability to human
neglect
patients. The model has been used to examine the neural mechanisms that
produce
neglect and recovery. These studies have focused mainly on the medial
agranular
cortex and its striatal projection zone, the dorsocentral striatum.
These
regions are components of a neural network for directed attention
analogous to
that found in primates. We are investigating the administration of
antibodies
to neurite inhibitory factors to induce axonal sprouting and recovery
from
neglect. Our studies indicate that the dorsocentral striatum may be the
crucial
site for the mechanisms which underlie recovery.
We have studied manatee brains and behaviors for 18 years. Our current
efforts
are focused on the tactile hairs that are distributed over the entire
body in
manatees. In other mammals, tactile hairs are generally limited to the
whisker
area of the face. In manatees this sytem may function as a distributed
array
for detecting water movements associated with the presence of other
animals,
river currents, and tidal flows. Manatees may use this system to orient
and
navigate in the murky waters they usually inhabit. We are investigating
the
function of this system using evoked brain potentials in captive
manatees. We
are also mapping the cortical locations of the representations for
tactile,
auditory and visual signals using neuroanatomical techniques.
Paul
J Reier,
Ph.D., Case-Western Reserve Univ., 1972
Primary
Department:
Neuroscience, COM
Research in this laboratory is directed at the cell biology of
neurons and
glia in the developing and injured peripheral and central nervous
systems with emphasis
on: mechanisms associated with neuronal outgrowth, axon-glial
interactions
during axonal elongation and myelinogenesis, PNS and CNS demyelination
and
remyelination, glial responses to neuronal injury, axon-glial
interactions, and
neural tissue transplantation; immunology of neural tissue
transplantation,
magnetic resonance imaging of neural tissue; neurophysiological and
behavioral
correlates of spinal cord injury and repair, neural tissue culture and
isolation of stem/progenitor cells from the adult CNS; ex vivo and in
vivo gene
delivery directed at neuronal rescue and regeneration in the injured
nervous
system; neural stem cell transplantation in CNS injury and repair.
The focus of all these interests is on translational (i.e.,
bench-to-bedside)neurobiology.
This laboratory in collaboration with other colleagues at the
University of
Florida were the first in this country to carry out a small clinical
trial
investigating the safety and feasibility of fetal neural tissue
transplantation
in people with a certain complication of spinal cord injury. Current
studies in
the laboratory continue to investigate the use of cells (i.e., stem or
stem-like cells) for repairing the injured spinal cord, and some
studies also
are moving towards the application of this therapeutic modality to
stroke. In
conjunction with transplantation, we also are testing the combined
effects of
other approaches including gene delivery, rehabilitation, and low-dose
irradiation. Some of these studies have also opened unexpected gateways
to
investigations pertaining to amyotrophic lateral sclerosis (Lou
Gehrig's
disease). Our overall goal is to find approaches that will optimally
combine
with native intrinsic repair processes (i.e., neuroplasticity) that can
lead to
improvement in function in spinal cord injury and other neurological
disorders.
Michael
E Robinson,
Ph.D.,
Primary
Department:
Clinical and Health Psychology, CHP
Recent work has been in the area of sex and gender role differences in pain perception. More broadly, my interests are in the contributions of social learning, negative affect, and personality factors in pain perception and in the interface between these factors and the ?first-order? biological contributions to pain perception. Most recently we have begun to use fMRI in the study of pain perception and placebo analgesia (with Nicholas Verne, Don Price, Richard Briggs, Bruce Crosson). My lab has also developed a number of clinically relevant pain stimulation protocols that combine laboratory psychophysics with clinically relevant stimulation. In addition to the research interests I have maintained an active practice of pain psychology and am clinically active in the pain clinics at UF.
Steven
N Roper,
M.D., Neurosurgery, UCLA, 1992
Primary
Department:
Neurological Surgery, COM
Dr. Roper's laboratory is centered on the cellular basis of
epilepsy. He
uses electrophysiology and in vitro brain slices as well as
histological
methods to accomplish this. He is trying to understand how in utero
insults
that alter normal cortical devlopment affect subsequent brain function
and
propensity to develop epilepsy. Dr. Roper also studies
electrophysiology of
hippocampal neurons obtained from people who undergo surgical treatment
for
medically intractable epilepsy. He tries to understand how changes in
this
tissue can lead to seizures and memory impairment in these patients.
Neil
E Rowland,
PhD,
Primary
Department:
Psychology, CLAS
Obesity and eating disorders: studies on the role
of
serotonin, endocannabinoids, and other neural systems in the control of
food
intake in rats and mice. We combine studies of food intake after either
acute
or chronic (to examine for tolerance) administration of select
pharmacological
agents with determination of regional brain activation, using Fos
immunoreactivity as a primary marker. The relationship between
suppression of
intake and development of learned flavor avoidances is also under
investigation, as is the use of flavor discriminations in this protocol
as a
model for study of cortical memory representations.
Alcohol and tobacco abuse: We are examining the role of stress, and in
particular early life stress on alcohol consumption in adulthood in
mice. In
collaboration with Dr Kem (UF Pharmacology) we are testing the effect
of novel
nicotinic antagonists agents as potential anti-smoking agents, using a
paradigm
in which rats are trained to discriminate nicotine from placebo, and
are
investigating the role of conditioned cues in self-administration..
Neuroeconomics: we are beginning to investigate the neural basis of simple decision-making in rodents subjected to different schedules and/or choices of reinforcement.
Dean
Sabatinelli,
PhD,
Primary
Department:
Psychology, CLAS
Using different brain mapping techniques (e.g., functional magnetic resonance imaging, dense electrode EEG), we are investigating the neural mechanisms underlying affective and attentional processing in people with and without diagnosable anxiety disorders. Drawing on an animal model of motivation, we are mapping the subcortical and cortical neural circuits involved in emotional perception and imagery. In addition to neural mapping, we measure autonomic and somatic indices of affective and attentional mobilization, using cardiovascular, electrodermal, electromyographic and respiratory measures. Taken together, our research is consistent with the hypothesis that affective cues activate basic motivational circuits that have evolved to mediate appetitive and defensive behaviors.
Susan
L Semple-Rowland,
Ph.D.,
Primary
Department:
Neuroscience, COM
Our research program is focused on the development
of
molecular-based therapies for treatment of inherited retinal diseases,
development of regulatable gene expression systems for use in viral
vector gene
therapy, identification and analyses of gene promoters that restrict
gene
expression to photoreceptor cells, and analyses of the function of
circadian
clocks in neural retina. Research techniques employed in our laboratory
include:
cDNA and cosmid library construction and screening
Northern and Southern blot
Relative RNA PCR
DNA sequence analysis
Viral vectors for gene therapy
SDS-PAGE
Two-dimensional gel electrophoresis
Western blot
Light and fluorescent microscopy
Histology - fluorescent and enzymatic visualization techniques
Embryonic retinal cell culture
Transient transfection analyses using various cell lines
Chemiluminescent transient transfection assays
GFP and nlacZ reporter gene analyses
Development and packaging of lentiviral vectors
Lentiviral-mediated analyses of promoter function in vivo
W.
Clay Smith,
PhD,
Primary
Department:
Ophthalmology, COM
The research in my lab centers on the molecules
involved in phototransduction--
the biochemical process by which photons are converted into a neural
signal.
The phototransduction enzyme cascade is an exquisitely sensitive
system, being
capable of producing a neural response to a single photon. This
responsiveness
is due largely to two aspects of the cascade. First, the cascade is
amplified
at each protein-protein interaction step producing (or hydrolyzing, as
the case
may be) literally millions of final effector molecules per second.
Secondly,
the inactivation of the cascade is tightly regulated at each
amplification
point such that the enzyme system is quickly quenched and returned to
the
responsive state. This tightly regulated system is a wonderful model
system
from which to study the visual process and also use as a model system
for other
G-protein-coupled receptor systems.
One of the many exciting things about phototransduction is that much of
the
process is conserved across ALL animals that have eyes, from the slimy
flatworms to the crunchy insects and right on up to humans. This means
that we
can use whatever organism is best suited for our studies to approach a
particular question regarding the visual cycle. Our lab currently has
experiments ongoing with humans, mice, rats, rabbits, frogs, alligators
(we are
at the
Our fundamental approach is a combination of molecular biology coupled
with
biochemistry and transgenic animal models. We do a lot of cloning work
directed
towards isolating components of the phototransduction system. From
there it's
on to site-directed mutagenesis and heterologous expression systems to
produce
enough protein to determine out how the components interact. These
interactions
then direct us towards transgenic models, introducing altered
components into
the visual cascade in vivo to provide the ultimate verification of our
results.
David
W Smith,
Ph.D., The
Primary
Department:
Psychology, CLAS
Our laboratories are actively involved in studies
of both
hearing and smell.
Current research projects in our auditory laboratories are concerned
with the
peripheral physiological and neural mechanisms underlying simple
perceptual
phenomena. These interests can be sub-divided into studies of the role
of the
descending, or olivocochlear efferent, neural system in normal,
acoustic
perception and perception resulting from electrical activation of the
auditory
system through a cochlear implant, or bionic ear. The efferent system
descends
from several areas of the mammalian brainstem to synapse on and
influence the
response of the outer hair cell receptors of the cochlea. Our work,
using
psychophysical and physiological measures in human and non-human
listeners,
characterizes the influence of this system on the perception of
transient
signals in noise and on selective auditory attention.
Our research with the cochlear implant seeks to characterize the
effects of
electrode design, electrode contact placement, contact configuration
and neural
survival on psychophysical and physiological measures of implant
performance in
non-human subjects.
Our olfactory laboratory is concerned with studies of olfactory
receptor neuron
transduction mechanisms. The laboratory employs operant olfactometers
to
characterize olfactory perception in genetically manipulated mice.
Donald
J Stehouwer,
Ph.D.,
Primary
Department:
Psychology, CLAS
My broad interests are in the areas of developmental and comparative psychobiology. The primary research focus of my laboratory is on neural remodeling during normal development, and how that remodeling generates adaptive behavioral development. We are also studying the mechanisms underlying recovery of function following spinal cord transection in neonatal rats, as well as the development of neural controls of locomotion in normal rats. A variety of neuroanatomical, electrophysiological, pharmacological and behavioral techniques are brought to bear on these problems, including microsurgery, electrophysiological recording, time lapse and frame-by-frame video tape analyses of movement, histological stains and tracers, and computer-assisted acquisition and analysis of electrophysiological and behavioral data.
Wolfgang
J Streit,
PhD,
Primary
Department:
Neuroscience, COM
Dr. Streit’s work has resulted in the following basic contributions to science: 1) Development of a histochemical procedure for staining microglial cells; 2) Development of a novel biological concept of ‘Functional plasticity of microglia’; 3) Extensive immunophenotypical characterization of activated microglia and perivascular macrophages; 4) Re-evaluation of the brain as an ‘immunologically privileged organ’ and concomitant development of the idea that microglia make up the brain’s endogenous immune system. These ideas have taken a foothold in neurobiology and they are widely accepted today. What is important for the future are the ramifications of these fundamental biological principles for understanding and treatment of neurological dysfunction and disease. In other words, what is the functional significance of reactive microgliosis. Dr. Streit has been a strong proponent of the idea that reactive microgliosis occurs in response to neuronal injury and/or dysfunction. He has endorsed the idea that neuron-derived signals trigger and regulate microglial activation and that it is neuron-microglia interactions that are essential for ensuring proper brain function, both physiologically and pathologically. Throughout his scientific career, he has promoted the philosophy that reactive microgliosis is a beneficial process that reflects the ability of the CNS to cope with the sequelae of injury and to maximize post-injury regeneration efforts. This point of view, which stands in contrast to the idea that microglial are autoaggressive immune effectors, reconciles the demonstrated immune effector function of microglia with the claim that an endogenous immune system of the brain must have evolved in order to protect this vulnerable organ from potentially detrimental side effects of a peripheral immune response. There are significant practical implications of these theories for CNS injury and disease. For example, it may be possible to repair axons transected as a result of spinal cord injury by using microglial cell transplants. It may also be possible to selectively stimulate microglia within the immunosuppressive environment of a brain tumor to become tumor cytotoxic effectors that can eradicate malignant glioma cells. Alzheimer’s disease could be a ‘microglial disease’, in the sense that as microglia age and become senescent they may be less able to carry out their normal neuroprotective functions, thus causing neurodegeneration through neglect.
Colin
Sumners,
Ph.D,
Primary
Department:
Physiology and Functional Genomics, COM
Neuro-related research within my group is focussed on the neural
mechanisms, within the brain, that are involved in stroke and
hypertension.
Current major areas of research are:
1. Understanding the potential neuroprotective role of angiotensin
receptors
during stroke. Our research has determined that angiotensin, acting via
its
type 2 (AT2) receptors, reduces neuronal death following conditions
that mimic
stroke in vitro. Our present studies are geared towards determining the
mechanisms of this neuroprotection, and the neuroprotective actions of
angiotensin in vivo. Methods include cell culture approaches, molecular
biology
and in vitro/in vivo gene transfer.
2. Understanding the role of macrophage migration inhibitory factor
(MIF)in
regulating angiotensin's actions within the brain. Angiotensin II has a
powerful pressor action mediated by its type 1 (AT1) receptors in the
hypothalamus and brainstem, and this action is enhanced in and
contributes to
high blood pressure. Thus, a major goal of our research has been to
define the
cellular actions of angiotensin in hypothalamic and brainstem neurons,
and
understand the factors that regulate angiotensinergic transmission in
normal
and hypertensive animals. Our studies have demonstrated that
angiotensin
induces the expression of MIF within the hypothalamus of normotensive
rats, and
that MIF acts as a negative feedback regulator of AT1 receptor-mediated
increases in neuronal firing. However, this MIF-dependent mechanism is
absent
in the hypothalamus of hypertensive rats. Our present studies are
geared
towards determining the mechanisms by which angiotensin induces MIF
expression
in normal rats, and why angiotensin fails to alter MIF expression in
hypertensive animals. Further, we aim to define the mechanisms of
action of MIF
on neuronal firing. Methods used include cell culture and whole animal
approaches, electrophysiology, molecular biology and in vitro/in vivo
gene
transfer.
Floyd
J. Thompson,
Ph.D.,
Primary
Department:
Neuroscience, COM
The research activities of my laboratory are directed towards
understanding
the neurobiology of the motor system following brain and spinal cord
injury. It
is our goal to acquire information that can direct the development of
specific
and effective therapies that can enhance the quality of life for
individuals
with these types of injuries. Our ongoing work addresses fundamental
neurophysiological changes in mechanisms that regulate reflex
excitability that
lead to the development of spasticity, and how these insights can guide
the
development of effective therapies. Currently these studies include a
comparison of two different types of therapeutic exercise to induce
activity-directed neuroplasticity of the motor system in the setting of
chronic
spinal cord injury. In our laboratory, one set of these studies is
being
conducted in a rodent model, with Dr. Prodip Bose serving as principal
investigator. In a parallel set of studies, we are collaborating with
Dr.
Andrea Behrman, Dept. of Physical Therapy, who is studying therapeutic
exercise
enhancement of basic neurophysiological mechanisms that influence human
locomotion following incomplete spinal cord injury. More recently, in
collaboration with the Dr. Ron Hayes Laboratory of the Center for
Traumatic
Brain Injury Studies at the McKnight Brain Institute, we are developing
a
traumatic brain injury (TBI) model to address several urgent issues
related to
the development and treatment of TBI-spasticity resulting from cortical
contusion injury. These studies have revealed new information regarding
the
nature, time course, and magnitude of spasticity following TBI. Ongoing
studies
utilizing this model will evaluate early intervention strategies that
could
intercept and decrease the severity of TBI-spasticity. Finally, in
collaboration with the Dr. Robert Yezierski and Dr. Robert Caudle
laboratories
of the
Nihal
Tümer,
Ph.D,
Primary
Department:
Pharmacology and Therapeutics, COM
The incidence of cardiovascular diseases increases in the elderly. In particular, the elderly do not regulate blood pressure as well as young people. The focus of our research is to investigate the loss of plasticity in catecholamine biosynthesis with age. The mechanisms involved in catecholamine biosynthesis, especially the induction of tyrosine hydroxylase (TH) are assessed at the molecular level by determining gene expression. In addition cAMP, cGMP-mediated as well as protein kinase-C signal transduction pathways in the peripheral and central nervous system are being investigated. Our goal is to understand the regulation of catecholamine biosynthetic enzymes and their role in hypertension, heart disease, stress and aging. Also, our recent interest centers on gene delivery, specifically GDNF, in hypothalamus to reverse the age-related decline in TH expression.
Krista
E Vandenborne,
PhD, Free
Primary
Department:
Physical Therapy, CHP
Dr Vandenborne’s work presents a multidisciplinary, integrated research approach to study muscle degeneration/regeneration from a pathophysiological level to functional impairment. The specific objectives of her program are to: 1) develop novel noninvasive techniques for the evaluation of skeletal muscle, 2) investigate the ability to enhance muscle function using modalities ranging from gene transfer, to exercise training and pharmacological treatment (hormonal supplement), and 3) examine the physiological process(es) essential to the repair of skeletal muscle and return of functional ability. Her current funded projects focus on the pathophysiology of muscle atrophy and muscle regeneration after limb disuse and the use of viral mediated gene transfer of IGF-I to enhance muscle rehabilitation.
Thomas W. Vickroy, Ph.D.,
Professor,
Primary department:
Physiological Sciences
The general research focus of my laboratory involves the neurochemical and molecular bases for chemically-mediated synaptic transmission in CNS pathways. Specific projects involve the following: (1) understanding the functional roles of presynaptic autoreceptors that regulate the release of acetylcholine, glutamate and other neurotransmitters; (2) understanding the role of glutamate transporters in the pathophysiological consequences of acute episodes of hypoxia and ischemia; (3) understanding the role of protein phosphorylation/dephosphorylation as a pathway for regulating transporter function; and (4) understanding cellular control mechanisms for regulating extracellular levels of excitatory transmitters during periods of heightened neuronal activity. The overall aim of these investigations is to obtain a more complete understanding of chemical neurotransmission and to identify molecular targets for drugs which may reverse specific changes brought about by certain diseases or neuropathological conditions.
Trainee Participation In this Research: Students involved with these research projects are trained to utilize a variety of techniques in order to gain a more thorough appreciation of the biochemical and molecular bases for neuronal communication. Students are trained to conduct a variety of investigations in isolated tissue preparations, including methods to investigate drug-receptor interactions, regulation of intraneuronal second-messenger molecules, and methods to assess the release, metabolism or uptake of various neuroactive compounds.
vickroyt@mail.vetmed.ufl.edu
Keith
D White,
PhD,
Primary
Department:
Psychology, CLAS
Imaging core of
Perceptual changes in psychiatric disorders: perceptual alternation
times
series, as from binocular rivalry or ambiguous figures, studied in
patients
with schizophrenia, bipolar disorder, or PTSD (for examples) and also
studied in
their relatives.
Charles
G Widmer,
DDS,
Primary
Department:
Orthodontics, COD
The general focus of my research program is in the area of masticatory muscle form and function and includes developmental features, functional architecture, motor control mechanisms, and mechanisms of muscle pain. Multiple species are examined including mouse, rabbit and human to adequately explore these topics. Sex-based differences are also an integral part of this work. The overall goal of these studies is to better understand the normal form and function of these muscles during development and in the adult. This work forms a basis for understanding pathological masticatory muscle conditions such as chronic muscle pain as well as re-innervation and repair after injury.
Charles
E Wood,
Ph.D.,
Primary
Department:
Physiology and Functional Genomics, COM
Present work in this laboratory focuses on three projects: 1) the interaction of prostanoids with the cardiovascular and endocrine controlling elements of the brain and the role of the locally-generated prostanoids in brain in the control of fetal stress responses (hypoxia and hypotension); 2) the influence of estrogen on the fetal brain regions which are important for cardiovascular and endocrine responsiveness to stress; and 3) the biological activity of sulfoconjugated estrogens in fetal plasma. This work is predicated on the observation that the fetal HPA axis is involved both in coordinating fetal stress responses (and thus is involved in the fetal survival of stress) and in coordinating the initiation of parturition. Identifying the basic neural mechanisms controlling fetal HPA function will yield a better understanding of both processes, as well as providing new strategies for therapeutic interventions. On this basic level, information gained in the ovine model will likely be directly applicable to the human being. We have found that prostaglandins generated within the fetal brain exert a profound influence on fetal HPA activity. The fetal response to hypotension, for example, is partially blocked using an inhibitor of prostaglandin biosynthesis. Hypotension stimulates the biosynthesis of the inducible form of the enzyme critically important for prostaglandin biosynthesis, cyclooxygenase-2 (COX-2), within the pathways in the fetal brain which impinge on the paraventricular nucleus, which sits at the head of the HPA axis. However, we have also reported that the expression of both COX-1 and COX-2 are increased in these regions as a function of development, supporting the notion that the increase in HPA axis activity which initiates parturition is itself dependent upon prostaglandin production. Recently, we have explored this ontogenetic regulation by demonstrating that fetal estrogen, which is released by the placenta prior to term, augments COX-2 expression in fetal brainstem and hypothalamus. Finally, we have initiated studies which demonstrate that estradiol-3-sulfate, the most abundant estrogen in fetal plasma, yet a steroid which has long been thought to be inactive, is converted in the fetal brain to its active form, 17ƒr-estradiol, where it increases HPA axis activity. All of these studies, which are funded on multiple extramural grants, will provide a more mechanistic understanding of fetal stress and parturition.
Updated 1/21/09