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Presenter Information

Seth Ronk

Location

SURC Room 137B

Start Date

15-5-2014

End Date

15-5-2014

Keywords

C. elegans, Serotonin, Behavior

Abstract

Understanding the neural basis for response to chronically elevated serotonin is important for pharmaceutical treatment of mood disorders, such as depression and schizophrenia. Chronic elevation of neurotransmitters can cause adaptation, or a diminished response, to the neurotransmitters. We have developed an assay which utilizes locomotion in the model organism Caenorhabditis elegans to study changes in genes/proteins involved in behavioral adaptation to serotonin. We have identified two mutant strains that fail to undergo adaptation to serotonin, protein kinase c-1 (pkc-1) and def-1. We also identified a novel phenotype in these mutants, depressed foraging. The purpose of this study is to characterize the cellular mechanisms by which pkc-1 modulates serotonin-dependent behavioral adaptation and to investigate the link of the depressed foraging phenotype and serotonin-dependent behavioral adaptation. Identification of cellular mechanisms that cause serotonin-dependent behavioral adaptation will further the understanding of how antidepressant drugs, which chronically elevate serotonin, influence the nervous system.

Faculty Mentor(s)

Carnell, Lucinda

Additional Mentoring Department

Biological Sciences

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May 15th, 12:00 PM May 15th, 12:20 PM

Characterizing PKC-1’s role in 5-HT dependent behavioral adaptation and depressed foraging, in Caenorhabditis elegans

SURC Room 137B

Understanding the neural basis for response to chronically elevated serotonin is important for pharmaceutical treatment of mood disorders, such as depression and schizophrenia. Chronic elevation of neurotransmitters can cause adaptation, or a diminished response, to the neurotransmitters. We have developed an assay which utilizes locomotion in the model organism Caenorhabditis elegans to study changes in genes/proteins involved in behavioral adaptation to serotonin. We have identified two mutant strains that fail to undergo adaptation to serotonin, protein kinase c-1 (pkc-1) and def-1. We also identified a novel phenotype in these mutants, depressed foraging. The purpose of this study is to characterize the cellular mechanisms by which pkc-1 modulates serotonin-dependent behavioral adaptation and to investigate the link of the depressed foraging phenotype and serotonin-dependent behavioral adaptation. Identification of cellular mechanisms that cause serotonin-dependent behavioral adaptation will further the understanding of how antidepressant drugs, which chronically elevate serotonin, influence the nervous system.