images Spring 2010 Neuroscience Seminars

Spring 2010 Seminar Series in Neuroscience

Location of Seminars: Muenzinger E214 (See map and directions)

Tuesday Feb 2, 4-5 pm

Dr. Dave Sherwood, Associate Professor, Department of Integrative Physiology, University of Colorado at Boulder

TITLE: Aiming Accuracy: What have we learned since Woodworth (1899)?

Abstract: The factors that affect accuracy in aiming movements has been a topic of interest in motor control since the work of Woodworth in the late 1800s. Early work in the area demonstrated the well-known speed-accuracy trade off where faster movements resulted in greater spatial errors. In the middle of the 20th century, research resulted in the development of FItts Law which demonstrated the relation between movement amplitude, target width, and movement time. More recently work has focused on the context in which movements are made. What happens to movement accuracy when two aiming movements are doing at the same time? What happens to movement accuracy when movements are made in a sequence? In summary, the talk will focus on the kinematic and contextual variables that affects movement accuracy.

Tuesday Feb 16, 4-5 pm Dr. Martin Sarter, Charles M. Butter Collegiate Professor of Psychology and Biopsychology Area Chair, Department of Psychology, University of Michigan

TITLE: "Acetylcholine, Attention, and Choline Transporters "

Abstract: The cortical cholinergic input system acts on the basis of second-long transients to mediate cue detection processes and associated attention mode shifts. This is a radical departure from conventional descriptions of the cholinergic system as a slowly acting neuromodulators system, mediating global “arousal” effects. The main components of the prefrontal circuitry that is largely responsible for the generation of these transients have been determined. Nicotinic acetylcholine receptor ligands modulate these transients and thereby affect cue detection efficacy and attentional performance. Finally, the import of choline into the presynaptic cholinergic terminal, via the high-affinity choline transporter, controls cholinergic and attentional capacities. The latter statement is based on evidence from mice hemizygous for the transporter and on preliminary evidence from humans heterozygous for a sub-capacity version of the transporter. Collectively, I will describe an explicit translational research program on the regulation and function of forebrain cholinergic systems.
Tuesday Mar 2, 4-5 pm

Dr. Marissa Ehringer, Assistant Professor, Department of Integrative Physiology, Institute for Behavioral Genetics, University of Colorado at Boulder

TITLE: “Underappreciated: Genes for the α6 and β3 neuronal nicotinic receptor subunits in human tobacco and alcohol behaviors

Abstract: Genes encoding neuronal nicotinic acetylcholine receptors (nAChRs) have become hot topics in human studies of nicotine behaviors, lung cancer, and other drugs, with over 30 publications examining the cluster including the CHRNA5/CHRNA3/CHRNB4 genes (Greenbaum et al, 2009).  Comparatively, little attention has been afforded the α6 and β3 neuronal nicotinic acetylcholine receptor (nAChR) subunits.  Receptors containing these are expressed on dopaminergic nerve terminals (reviewed in Grady et al, 2009), and model systems have provided evidence that alcohol may modulate the pharmacological properties of nicotine binding at nAChRs (reviewed in Schlaepfer et al, 2008). A few human genetic studies have examined the human CHRNA6/CHRNB3 gene cluster and found evidence for association with nicotine dependence (Bierut et al., 2007; Hoft et al., 2008; Saccone et al., 2007) and early subjective response to nicotine (Zeiger et al., 2008; Ehringer et al.; 2009). Our group has also reported an association between CHRNA6 and alcohol use, specifically average number of drinks per day (Hoft et al., 2009).  We have recently replicated this association in an extended sample of our first study, and in an independent sample of adolescents/young adults.  Now we are taking two approaches to examine the possible functional implications of these human genetic associations.  First, in vitro molecular genetics assays are being conducted to examine whether different variants in the CHRNB3 promoter region may lead to differences in gene expression.  Results indicate that variation in this region may be important in regulating expression of the β3 subunit (Ehringer et al, 2009).  Second, α6 and β3 knock-out mice are being tested for a variety of alcohol-related behaviors.  Preliminary data suggest that mice lacking the β3 subunit may differ in measures of initial sensitivity to alcohol.  By integrating findings from human genetic studies into molecular and animal behavior genetics approaches, we hope to improve our understanding of how variation in the CHRNB3/CHRNA6 genes lead to increased risk for nicotine and alcohol problem behaviors, with the long-term goal of improving prevention and treatment of these disorders.


Dr. Ron Duman, Yale



Tuesday April 6, 4-5 pm

Dr. Ken McCarthy, Professor, Department of Pharmacology, University of North Carolina at Chapel Hill Medical School

TITLE: Sorting Out Astrocyte Physiology from Pharmacology “TBA”

Abstract: Astrocytes are the predominate cell type in the brain, closely associate with other neural cell types, exhibit a wide array of neurotransmitter receptors, respond to neuronal activity, and release neuroactive molecules; in spite of this, we know very little about the role of these cells in physiology, behavior, or disease. A major limitation in this area is the lack of models that permit the study of astrocyte function in neural systems following physiological stimulation. To date, nearly all studies of astrocytic function have relied on pharmacological approaches to activate these cells and to record the effects of their activation in situ. For example, our laboratory was the first to demonstrate that electrical stimulation of the Schaffer collateral pathway leads to astrocytic calcium responses in the CA1 region if the hippocampus. However, the degree to which this occurs during normal hippocampal activity remains unclear. Similarly, our laboratory was the first to use caged IP3 to demonstrate that the selective activation of hippocampal astrocytes led to gliotransmitter release and the modulation of synaptic transmission in situ. However, subsequently we found that the selective activation of astrocytic GPCRs linked to calcium mobilization fails to cause gliotransmitter release or effect synaptic transmission. These findings have resulted in a significant controversy in this area and bring into question the pharmacological approaches that have been used by us and others to study astrocytes in vitro and in situ. The focus of my talk will be one whether astrocytes release gliotransmitters that modulate synaptic transmission and plasticity. In addition, I will discuss new genetic approaches for selectively activating astrocytic signaling cascades in vivo that enable us to investigate the role of astrocytes in behavior.

Tuesday April 20, 4-5 pm

Dr. Susan Patterson, Assistant Professor, Department of Psychology and Neuroscience, University of Colorado at Boulder

TITLE: Synaptic and Molecular Mechanisms of Increased Cognitive Vulnerability with Aging Revisiting the Role of BDNF“TBA”