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Fall 2004 Seminar Series in Neuroscience
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| Tuesday Sept 14, 4-5 pm |
Dr.
Randy Ross, University of Colorado, Health Sciences
Center
Title: Hypothesis: a
prenatal nutritional supplement as a primary prevention
strategy in schizophrenia
Abstract:
The alpha7 nicotinic receptor gene alters early brain
development, which alters physiological function, which
changes attentional abilities, which is associated with
risk for schizophrenia. From gene to disease, we will
review the role of nicotinic mechanisms in schizophrenia
and discuss the translation of this knowledge into a
possible primary prevention strategy.
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| Tuesday Sept 28, 4-5 pm |
Dr.
Stuart Tobet, Department of Biomedical Sciences, Colorado
State University
Title: Mammalian hypothalamus:
Sex and development
Abstract:
Steroid hormones dramatically influence the development
of numerous sites in the nervous system. Basic mechanisms
in neural development provide foci for understanding
how factors related to sex can alter the ontogeny of
these regions. Sex differences in neurogenesis, cell
migration, cell differentiation, cell death, and synaptogenesis
are being addressed. Any and all of these events serve
as likely targets for genetic or gonadal steroid-dependent
mechanisms throughout development. Although the majority
of sexually dimorphic characteristics in brain have
been described in older animals, many hormonal mechanisms
that determine sexually differentiated brain characteristics
occur during critical perinatal periods. It is likely
that transient molecular events set the stage for later
amplification by hormone actions. Sex differences in
the positioning of cells in the developing hypothalamus
further suggest that cell migration may be one key target
for early gene actions that impact long-term susceptibility
to brain sexual differentiation.
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| Tuesday Oct 12, 4-5 pm |
Dr.
Robert Sutherland (Canada)
Title: A behavioural
analysis of the role of the hippocampus in long-term
memory
Abstract:The idea that
the hippocampus temporarily stores episodic memories
until other regions of cortex form permanent memories
has faced serious recent challenges. A series of experiments
measuring retrograde amnesia after damage to the hippocampus
shows that this view of memory is wrong and a reconceptualization
will be presented based upon interactions between multiple
long-term memory systems.
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| Week of Tuesday Oct 26 |
No
Seminar Scheduled — Annual Society for Neuroscience
Meeting, San Diego, CA
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| Tuesday Nov 2, 4-5 pm |
Dr.
Shu-Chan Hsu, Department of Cell Biology & Neuroscience,
Rutgers University
Title: The role of exocyst
complex in neuronal development
Abstract:
A key initial step in the establishment of neuronal
network is the outgrowth of neurites, a complex process
that requires coordinated cytoskeleton remodeling and
vesicle targeting to the plasma membrane. Recent work
from my laboratory and from other labs suggests that
the exocyst, a 734 kDa multisubunit protein complex,
is essential for neurite outgrowth and regulation of
vesicle trafficking in response to cellular signals.
Based on this criterion, defining the function of the
exocyst complex and using it as a molecular handle to
identify other important components of the neurite outgrowth
process has become the focus of my laboratory research.
Three major approaches have been used to define the
molecular mechanisms of exocyst function. First, we
have generated highly specific antibodies to investigate
correlations between endogenous exocyst distribution
and outgrowth of neurites. Second, we characterized
the molecular associations of the exocyst complex and
their role in neurite outgrowth. Third, we set up in
vitro protein binding/activity assays and in vivo transfection
studies to determine the role of exocyst and its associated
proteins in regulating neurite outgrowth. Based on our
results we hypothesize that a role underlying exocyst’s
function in promoting neurite outgrowth involves modulating
cytoskeleton dynamics.
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| Tuesday Nov. 16, 4-5 pm |
Dr.
David
Diamond, Department of Psychology, University of South
Florida
Title: How does stress
affect the hippocampal-prefrontal memory system
Abstract:
The effects of stress on memory are complex. Intense
stressful experiences, such as combat and assault, can
produce memories that are so pathologically strong that
they can interfere with the quality of life for people
decades after the traumatic experience occurred. It
is also a common occurrence that stress can cause people
to be forgetful. How can stress enhance and also impair
memory? This lecture will provide behavioral, pharmacological
and molecular perspectives on stress-memory interactions,
with a discussion of the involvement of the hippocampus,
prefrontal cortex and amygdala in the modulation of
memory by stress.
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| Tuesday Nov 30, 4-5 pm |
No
seminar scheduled on account of Front
Range Neuroscience Group Meeting in Fort Collins.
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| Tuesday Dec 7, 4-5 pm |
Dr.
Jack
Kinnamon, Department of Psychology, Denver University
Title: Rats with Good
Taste
Abstract:
The vertebrate taste bud is a dynamic system in which
all of the cells are replaced approximately every 10
days to two weeks. During that time a given taste receptor
cell matures, forms synaptic connections with sensory
nerve fibers, performs its sensory functions, and then
goes into senescence and dies. The taste bud is an amazing
sensory organ. A typical mammalian taste bud contains
approximately 100-150 cells, but is able to distinguish
sweet, sour, salty, bitter and amino acids. While other
sensory systems (e.g., auditory, olfactory, visual)
use only one sensory transduction pathway, the gustatory
system utilizes a variety of sensory transduction mechanisms.
Gustatory receptor cells generate action potentials
and convey the sensory information to the cranial nerves
via chemical synapses. This is especially interesting
because the gustatory receptor cells are epithelial
and not neural in origin. My laboratory is studying
how the taste receptor cells talk to the cranial nerves.
We are especially interested in the synaptic proteins
involved in the docking, fusion and exocytosis of synaptic
vesicles.
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