Columbia University in the City of New York

Nov 27, 20184:00 pm
Seminar

Prefrontal Cortex versus. V1: Profound Differences That Confer Cognitive Vulnerability

Featuring Amy F.T. Arnsten, PhD, Professor of Neuroscience, Psychiatry, Psychology and the Child Study Center, Yale University School of Medicine.

November 27th, 4:00 pm – 5:00 pm at the Neurological Institute of New York (1st floor)

This seminar will be held in the Neurological Institute of New York's Auditorium (1st floor). Columbia University's Intercampus Shuttle Service is the best way to travel between campuses.

The association cortices atrophy in cognitive disorders such as schizophrenia and Alzheimer’s Disease, while the primary visual cortex (V1) is more resilient. What makes the association cortices so vulnerable? Dr. Arnseten and her team have been comparing the neurons that subserve visuo-spatial working memory in the primate dorsolateral prefrontal cortex (dlPFC), to neurons in V1 that respond to visual stimuli, and have found marked differences in both neurotransmission and modulation. Neurons in V1 show classic responses: they rely heavily on AMPAR neurotransmission, and cAMP signaling enhances neuronal firing, likely by increasing glutamate release. In contrast, dlPFC neurons have little reliance on AMPAR, and instead depend on cholinergic permissive effects on NMDAR transmission. These neurons are very dependent on arousal state, and feedforward, cAMP-calcium signaling increases K+ channel opening to reduce firing, e.g. during stress. Dysregulation of cAMP-calcium signaling with advancing age leads to loss of neuronal firing and impaired working memory, as well as tau phosphorylation. Dysregulated calcium-cAMP signaling and tau hyperphosphorylation are also seen in the aging entorhinal cortex, the cortical area most vulnerable in Alzheimer’s Disease. These data show how studies of the primate cortex can help to illuminate the etiology of cognitive disorders.

Dr. Arnsten is Professor of Neuroscience at Yale Medical School, with joint appointments in Psychiatry, Psychology and the Yale Child Study Center. She is one of the few scientists studying the molecular regulation of higher cortical circuits in primates, and how altered signaling confers vulnerability to cognitive disorders. Arnsten received her undergraduate degree in Neuroscience from Brown University in 1976, and her PhD in Neuroscience from UCSD in 1981. She did a brief post-doctoral fellowship with Susan Iversen at Cambridge University, UK, before becoming a post-doctoral fellow with Patricia Goldman-Rakic at Yale. Arnsten is a member of the National Academy of Medicine, and the recipient of the Goldman-Rakic Prize for Outstanding Research in Cognitive Neuroscience from the Brain and Behavior Research Foundation. Her work in animals has successfully translated to human therapies: guanfacine (Intuniv™) for the treatment of ADHD and related prefrontal cognitive disorders, and prazosin for the treatment of PTSD.

Those who wish to meet the speaker during their visit should contact Shushruth Fnu (Shadlen Lab). For general inquiries please contact [email protected].

The Columbia Neuroscience Seminar series is a collaborative effort of Columbia's Zuckerman Institute, the Department of Neuroscience, the Doctoral Program in Neurobiology and Behavior and the Columbia Translational Neuroscience Initiative, and with support from the Kavli Institute for Brain Science.

Venue: the Neurological Institute of New York (1st floor)
710 W 168th St, New York, NY 10032

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