Event Title

Effect of 4-methyloctanoic acid Treatment on C. elegan Model for Juvenile Epilepsy

Presenter Information

Carolyn Ornato, Biotechnology

Faculty Sponsor(s)

Susan Swope

Location

Hartman Union Building Courtroom

Presentation Type

Event

Start Date

4-28-2017 4:00 PM

End Date

4-28-2017 5:00 PM

Abstract

Nicotinic acetylcholine receptors mediate fast signal transmission at synapses through ion channels. Inhibition causes defects in human sodium channel proteins, which cause numerous disorders. A deletion in the neuronal acetylcholine receptor subunit alpha-7 (CHRNA7) results in juvenile myoclonic epilepsy and genetically transmitted schizophrenia. C. elegans, which have a similar genome to humans, have a gene known as Deg-3. In C. elegans this gene encodes, and is homologous to CHRNA7, for an alpha subunit of a nicotinic acetylcholine receptor. Inhibition of DEG-3 causes a gain-of-function mutation resulting in neurological degeneration and uncoordinated movements. Using RNAi, a vector was created and given to C. elegans to induce the DEG-3 mutation. One group of worms was treated with 4-methyloctanoic acid, which is known to eliminate epilepticus in animals and increase suppression of pentylenetetrazol (PTZ)-induced epileptiform discharges in vitro. The untreated worms have shortened life spans and population-wide incoordination. The worms treated with 4-methyloctanoic acid had increased life span and the incoordination was seen only later in their life span, or not at all. This research will encourage further research into the use of 4-methyloctanoic acid as a seizure control treatment.

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Apr 28th, 4:00 PM Apr 28th, 5:00 PM

Effect of 4-methyloctanoic acid Treatment on C. elegan Model for Juvenile Epilepsy

Hartman Union Building Courtroom

Nicotinic acetylcholine receptors mediate fast signal transmission at synapses through ion channels. Inhibition causes defects in human sodium channel proteins, which cause numerous disorders. A deletion in the neuronal acetylcholine receptor subunit alpha-7 (CHRNA7) results in juvenile myoclonic epilepsy and genetically transmitted schizophrenia. C. elegans, which have a similar genome to humans, have a gene known as Deg-3. In C. elegans this gene encodes, and is homologous to CHRNA7, for an alpha subunit of a nicotinic acetylcholine receptor. Inhibition of DEG-3 causes a gain-of-function mutation resulting in neurological degeneration and uncoordinated movements. Using RNAi, a vector was created and given to C. elegans to induce the DEG-3 mutation. One group of worms was treated with 4-methyloctanoic acid, which is known to eliminate epilepticus in animals and increase suppression of pentylenetetrazol (PTZ)-induced epileptiform discharges in vitro. The untreated worms have shortened life spans and population-wide incoordination. The worms treated with 4-methyloctanoic acid had increased life span and the incoordination was seen only later in their life span, or not at all. This research will encourage further research into the use of 4-methyloctanoic acid as a seizure control treatment.