Fall 2009 Seminar Series in Neuroscience
Location of Seminars: Muenzinger E214 (See map
|Tuesday Sept 15, 4-5 pm
Julie Fiez, Professor, Department of Communication
Sciences & Disorders, University of Pittsburgh
of Making a Decision: Feedback Signals and Learning"
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.
|Tuesday Sept 29, 4-5 pm
Justin Rhodes, Assistant Professor, Department
of Psychology, University of Illinois at Urbana-Champaign
Title: " The Functional
Significance of Exercise-Induced Adult Hippocampal Neurogenesis"
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.
|Tuesday Oct 13, 4-5 pm
Denis Pare Rutgers University
Basis of Safety Learning in the Amygdala"
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.
|Tuesday Nov 3, 4-5 pm
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
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.
|Tuesday Nov, 17, 4-5 pm
Alaa Ahmed, Assistant Professor, Dept.
of Integrative Physiology, University of Colorado at
representations of dynamics for movement and posture"
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.
|Tuesday Dec 8, 4-5 pm
Institute of Behavioral Genetics, University of Colorado
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.