In order to celebrate the start of the academic year and welcome our new
graduate students, postdocs, and research staff members, I would like to
invite you to participate in an IBG Orientation and Poster Day, on Friday,
August 22th. As in past years, this will be an opportunity for IBGers to
get together for an afternoon of stimulating conversation. It will also
introduce the new members of our Institute to the breadth of research
conducted at IBG.
I hope that you will be able to participate. If so, please bring posters
that you, or members of your lab, have presented during the past year and
mount them between 8:00 a.m. 3:00 p.m. on Friday, the 22th. A list of
board assignments will be posted outside room 255 late Thursday afternoon.
As usual, we will provide mounting supplies. The poster session will be
held from 3:00 to 5:00 p.m. and will be an informal gathering with no set
time for manning the posters that will be left to your discretion.
Refreshments will be served during the session.
This year, Elaine Pauly is assisting with the coordination of the poster
session. Please let Elaine know, as soon as possible, how many posters you
or your group would like to display. That information will be helpful in
case we need to rent additional poster boards. She can be reached at
extension 2-2831 (303 492 2831 for those of you in Denver), or at
Paulye@Colorado.edu.
I look forward to seeing your posters later this month, and thank you in
advance for your efforts in making this both a fun and stimulating IBG
event.
Cordially,
Toni Smolen
Seminar
Tuesday, August 5
4:00 PM - 5:00 PM
IBG 120
Nandita Mitra, PhD
Assistant Professor University of Pennsylvania
Department of Biostatistics & Epidemiology
Analysis of Population Based Genetic Association Studies
Using Propensity Score Methods
Please join us for refreshments at 3:45 pm
University of Colorado (East Campus)
Institute for Behavioral Genetics
1480 30th Street, Room 120
Boulder, CO 80303
Colloquium
Friday, June 6
4:00 PM - 5:00 PM
IBG 120
Henry A. Lester, Ph.D.
Bren Professor of Biology Department of Neuroscience
Division of Biology
California Institute of Technology
Pasadena, California
Changes in the Brain During Chronic Nicotine
Several nicotinic ACh receptor (nAChR) subtypes modulate dopamine release,
and therefore may be drug targets for disorders such as nicotine
dependence and Parkinson's disease. Receptors containing 6 nAChR
subunits ( 6*) are highly expressed in midbrain dopamine neurons, and are
implicated in cholinergic modulation of dopamine release and the response
to nicotine. We generated mutant mice expressing hypersensitive 6*
receptors to selectively isolate and amplify physiological and behavioral
responses to 6 activation. Midbrain dopamine neurons from mice
expressing Leu9'Ser (L9'S) 6* receptors exhibit markedly hypersensitive
nicotinic currents and fire action potentials in response to 6
activation. In midbrain, functional 6* nAChRs are selectively expressed
in dopamine, but not GABA, neurons. On the other hand, ?4* receptors are
expressed both in dopamine neurons and in the GABA neurons that inhibit
the dopamine neurons. The previously described hypersensitive ?4Leu9'Ala
strain allows selective activation of ?4* receptors by nicotine.
Selective activation of 6* nAChRs in vivo stimulates locomotor activity
via striatal dopamine release. However, selective activation of ?4* in
vivo inhibits locomotor activity, presumably because the dominant action
is the inhibition produced by GABA neurons. This is the first study to
report selective 6 activation in vitro and in vivo, and suggests the
potential of targeting 6* receptors for neural disorders involving
dopamine transmission.
Wednesday, April 2
4:00 PM - 5:00 PM
Muenzinger E214
Thomas J. Gould, Ph.D.
Associate Professor of Psychology and the Center for Substance Abuse
Research
Temple University
Nicotine and Learning: From Behavior to Neural and Genetic Substrates
Tobacco use is a serious health problem in the United States, which
attests to the strong addictive nature of nicotine. Whereas nicotine is
reinforcing, it is not as reinforcing as other substances of abuse. This
suggests that additional factors may contribute to nicotine addiction.
Nicotinic acetylcholinergic receptors have been linked to cognitive
processes; thus the ability of nicotine to alter learning and synaptic
plasticity may facilitate nicotine addiction. Research in the Gould
laboratory links the effects of nicotine on hippocampus-dependent learning
to underlying changes in neural and genetic substrates and examines how
these effects change as nicotine administration transitions from acute
treatment to chronic treatment to withdrawal from chronic treatment.
Because both learning and addiction result in long-lasting behavioral
changes, understanding the cellular and genetic factors that contribute to
these changes in plasticity and behavior will advance understanding of
both addiction and learning.
Pharmacology and Genetics of Sleep Disorders: Insights from animal
models
The neurobiological underpinnings of sleep and its disorders remain
ill-defined. I and my colleagues have utilized pharmacological and
behavioral manipulations of wild type and genetically engineered
animals and have exploited phenotypic variability among
laboratory mouse strains to gain insights in this area. In my
presentation, I will describe the knowledge we have gained regarding
mechanisms of sleep/wake therapeutics, the interactions of the
molecular circadian clock with sleep regulatory mechanisms, and a
unique animal model we have developed for studies on circadian
regulation of sleep.
Wednesday, April 16
4:00 PM - 5:00 PM
Muenzinger E214
Dr. Don Cooper
Assistant Professor
University of Texas Southwestern Medical Center
Psychostimulant-induced plasticity in the brain reward circuitry: From
measurement to manipulation
Drug addiction is primarily a disease that targets the brain*s
motivation/reward and decision-making centers. Addicts demonstrate a loss
of control over drug intake and often seek drugs even in the face of
profound negative consequences. Such impairments in decision-making are
hallmark features of pathological frontal cortical function. The goal of
the Cooper laboratory is to use state-of-the-art functional analysis and
novel molecular genetic tools to identify the mechanisms of
psychostimulant-induced plasticity in the brain reward pathways and then
use these tools to restore normal cellular function. Recently, the Cooper
laboratory has explored a reverse translational (human to rodent) approach
to uncover a novel mechanism for diminished prefrontal cortical function
(hypofrontality) during abstinence from cocaine. A combination of brain
imaging in cocaine addicts, rodent DNA microarray analysis, transgenic GFP
mice and multielectrode electrophysiological recordings reveal
cocaine-induced molecular and physiological changes in prefrontal cortical
superficial layer function. Such prefrontal cortical layer specific
neuroadaptations may be shared across addictive substances and, therefore,
may be a useful therapeutic target. Using rodent cocaine
self-administration as a model to induce plasticity, the Cooper laboratory
is now focused on restoring cocaine-induced prefrontal cortical synaptic
function using viral vectors and novel AMPAkine compounds that target
superficial prefrontal cortical layers to boost excitatory transmission.
Marilyn E. Coors, PhD
Assistant Professor of Bioethics and Genetics
Department of Psychiatry and the
Center for Bioethics & Humanities
University of Colorado Denver
"The Interface of Bioethics and Psychiatric Genetic Research"
