Using Caenorhabdidtis elegans to understand the cellular mechanisms of serotonin-dependent behavioral adaptation

Presenter Information

Seth Ronk

Document Type

Oral Presentation

Campus where you would like to present

SURC Ballroom C/D

Start Date

16-5-2013

End Date

16-5-2013

Abstract

Behavior of an organism is created and controlled by the signaling within and between neurons throughout the nervous system. In higher organisms the complexity of the nervous system is difficult to understand. Therefore, due to a simple nervous system made up of only 302 neurons we use Caenorhabditis elegans, a microscopic soil nematode, as a model organism to understand how neurons and neuronal circuitry function. Serotonin (5-HT) is an important neurotransmitter that modulates mood, sleep, and appetite. 5-HT signaling is poorly understood on a cellular level and dysfunction in serotonin-dependent signaling is associated with illnesses such as depression and insomnia. We investigated the mechanisms involved in serotonin-dependent behavioral adaptation. We have found that overnight exposure to 3 mg/ml 5-HT results in a recovery of speed from the inhibitory acute effect on locomotion. Acute exposure results in speeds of 35 μm/s that increases to 140 μm/s after adaptation, which is a 60 percent recovery of untreated control speed (215 μm/s). We identified a mutant that is defective in adaptation to 5-HT. Animals deficient in the gene pkc-1, similar to a mammalian gene for PKC, are defective in recovery of speed to chronic exposure to 5-HT. The pkc-1 mutant produces adaptation speeds of 16 μm/s, which are similar to acute speeds 14 μm/s. These results offer insight to a cellular pathway that is involved in 5-HT-dependent behavioral adaptation.

Poster Number

35

Faculty Mentor(s)

Lucinda Carnell

Additional Mentoring Department

Biological Sciences

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May 16th, 8:20 AM May 16th, 10:50 AM

Using Caenorhabdidtis elegans to understand the cellular mechanisms of serotonin-dependent behavioral adaptation

SURC Ballroom C/D

Behavior of an organism is created and controlled by the signaling within and between neurons throughout the nervous system. In higher organisms the complexity of the nervous system is difficult to understand. Therefore, due to a simple nervous system made up of only 302 neurons we use Caenorhabditis elegans, a microscopic soil nematode, as a model organism to understand how neurons and neuronal circuitry function. Serotonin (5-HT) is an important neurotransmitter that modulates mood, sleep, and appetite. 5-HT signaling is poorly understood on a cellular level and dysfunction in serotonin-dependent signaling is associated with illnesses such as depression and insomnia. We investigated the mechanisms involved in serotonin-dependent behavioral adaptation. We have found that overnight exposure to 3 mg/ml 5-HT results in a recovery of speed from the inhibitory acute effect on locomotion. Acute exposure results in speeds of 35 μm/s that increases to 140 μm/s after adaptation, which is a 60 percent recovery of untreated control speed (215 μm/s). We identified a mutant that is defective in adaptation to 5-HT. Animals deficient in the gene pkc-1, similar to a mammalian gene for PKC, are defective in recovery of speed to chronic exposure to 5-HT. The pkc-1 mutant produces adaptation speeds of 16 μm/s, which are similar to acute speeds 14 μm/s. These results offer insight to a cellular pathway that is involved in 5-HT-dependent behavioral adaptation.