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 ircadian 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.
