Fall 2009 Seminar Series in Neuroscience

Dr. Julie Fiez, Professor, Department of Communication Sciences & Disorders, University of Pittsburgh

Title:"The Consequences of Making a Decision: Feedback Signals and Learning"

Abstract: The past decade has seen renewed interest in the neural substrates associated with reward processing. Much of the attention has focused on the ventral portions of the basal ganglia and the idea that learning signals mediated by dopamine neurons signal errors in reward prediction. In this talk, we will instead focus on reward-related processing in the dorsal portion of the basal ganglia. I will argue that when humans make a cognitive decision that is followed by feedback, the dorsal striatum is able to use this outcome information to reshape the cortical representations that guide performance. These ideas are being tested through a new study involving arithmetical training in college students.

Dr. Justin Rhodes, Assistant Professor, Department of Psychology, University of Illinois at Urbana-Champaign

Title: " The Functional Significance of Exercise-Induced Adult Hippocampal Neurogenesis"

Abstract: Before the 1990s, people widely thought that once you become an adult your brain cells cannot regenerate. Therefore, it was thought that if your neurons die, they can never be replaced. Now we know that there are at least two regions in the adult human brain that continue to incorporate new neurons throughout life, the olfactory bulb and the dentate gyrus of the hippocampus. This discovery has generated great excitement and enthusiasm, because it we can understand how neurons regenerate and incorporate into networks in the adult brain, that could have broad applications for treatment of neurodegenerative disease, cognitive decline with aging, stroke, and possibly depression and anxiety. Moreover, the fact that the hippocampus is one of the regions that has retained the ability to regenerate neurons throughout life is intriguing because of the important role of hippocampus in learning and memory. Nonetheless, despite great progress identifying the factors that can regulate adult hippocampal neurogenesis such as diet, sex, genetics, age, hormones, trophic factors, growth factors, breeding season, alcohol exposure, stress, depression, exercise, environmental enrichment, little is known about the functional significance. The talk will review recent progress discovering the functional significance of exercise-induced hippocampal neurogenesis in mice as a model organism.

Dr. Denis Pare Rutgers University

Title: "Synaptic Basis of Safety Learning in the Amygdala"

Abstract: Anxiety disorders such as post-traumatic stress are characterized by an impaired ability to learn that cues previously associated with danger no longer represent a threat. However, the mechanisms underlying fear extinction remain unclear. My talk will present evidence that extinction depends on increased levels of synaptic inhibition in fear output neurons of the central amygdala. This increased inhibition results from the reinforcement of fear input synapses to GABAergic intercalated amygdala neurons that project to CE. Overall, our results suggest that intercalated cells constitute a promising target for pharmacological treatments aiming to facilitate the treatment of anxiety disorders.

Dr. Pei-San Tsai, Associate Professor, Dept. of Integrative Physiology, University of Colorado at Boulder

Title: "FGF Signaling: A common tie between olfactory morphogenesis and reproductive failure"

Abstract: Gonadotropin-releasing hormone (GnRH) produced by a small population of neurons is indispenable for driving vertebrate reproduction. Neurons that produce GnRH have a very peculiar embryonic origins in that they arise in the nose. Therefore, disruption of the olfactory development almost always leads to the disruption of GnRH neurons, resulting in a double-whammy effects: absence of smell and inability to reproduce, a pathology called Kallman syndrome. Using transgenic mice, we have identified a number of signaling pathways that, when deficient, lead to the simultaneous disruption of GnRH neuron development and olfactory structures. Further, the mutations in these signaling genes have been identified in Kallman syndrome and other reproductively deficient patients. This talk will discuss the mechanisms by which these pathways regulate the development of the nose, including GnRH neurons.

Dr. Alaa Ahmed, Assistant Professor, Dept. of Integrative Physiology, University of Colorado at Boulde

Title: "Flexible representations of dynamics for movement and posture"

Abstract:The effortless ease with which we move and interact with objects in our environment masks the true complexity of the control processes involved. In order to manipulate an object skillfully, the brain must learn its dynamics, specifying the mapping between applied force and motion. Further difficulty arises, in part, from the necessity to use complex objects and to move between multiple postures, many of which are unstable. How this mapping changes with object complexity and postural instability is a fundamental issue in sensorimotor control. In this talk I will present results showing that object dynamics can be flexibly represented in different coordinate frames by the brain, depending on object complexity. This suggests that with experience, the representation dynamics of a manipulated object may shift from a coordinate frame tied to the arm towards one linked to the object. I will also show recent results suggesting that the brain maintains flexible representations of novel object dynamics in different postural configurations with varying stability requirements. The additional effort required to maintain such flexible representations would be economical because such a representation allows for object use regardless of object orientation in the hand, whole-body posture, and instability in the environment.

Dr. Chris Link, Institute of Behavioral Genetics, University of Colorado at Boulder

Title: “Modeling aspects of Alzheimer's Disease using C. elegans”

Abstract:Alzheimer's disease (AD) is a progressive dementia characterized by the accumulation of extracellular senile plaques in the brain.  A major component of senile plaques is the beta-amyloid peptide, and genetic evidence suggests this peptide is centrally involved in AD pathology.  However, the mechanisms of beta-amyloid peptide neurotoxicity, and the specific toxic form of the peptide, remain controversial.  We have generated an in vivo model of beta amyloid peptide (Abeta) toxicity by genetically engineering the nematode worm C. elegans to express (human) Abeta.  This model has allowed us to do an in vivo structure/function analysis of Abeta toxicity by assaying the effects of specific amino acid substitutions in Abeta expressed in C. elegans.  These studies have been complemented by cell culture experiments using adenovirus transfection or exposure of cells to synthetic Abeta peptide.  Our results support the hypothesis that Abeta toxicity involves oligomeric forms of Abeta that specifically damage membranes.  We have also used the C. elegans model to investigate the epidemiological finding that coffee consumption is protective against Alzheimer's (and Parkinson's) diseases.   We find that multiple components in coffee extracts are protective against Abeta toxicity in C. elegans, and this protection is due to activation of a specific conserved pathway.