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Risley MG, Kelly SP, Jia K, et al. Modulating Behavior in C. elegans Using Electroshock and Antiepileptic Drugs. PLoS One. 2016;11(9):e0163786doi: 10.1371/journal.pone.0163786.
Risley, M. G., Kelly, S. P., Jia, K., Grill, B., & Dawson-Scully, K. (2016). Modulating Behavior in C. elegans Using Electroshock and Antiepileptic Drugs. PloS one, 11(9), e0163786. https://doi.org/10.1371/journal.pone.0163786
Risley, Monica G, et al. "Modulating Behavior in C. elegans Using Electroshock and Antiepileptic Drugs." PloS one vol. 11,9 (2016): e0163786. doi: https://doi.org/10.1371/journal.pone.0163786
Risley MG, Kelly SP, Jia K, Grill B, Dawson-Scully K. Modulating Behavior in C. elegans Using Electroshock and Antiepileptic Drugs. PLoS One. 2016 Sep 26;11(9):e0163786. doi: 10.1371/journal.pone.0163786. eCollection 2016. PMID: 27668426; PMCID: PMC5036823.
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PLoS One. 2016 Sep 26;11(9):e0163786. doi: 10.1371/journal.pone.0163786. eCollection 2016.

Modulating Behavior in C. elegans Using Electroshock and Antiepileptic Drugs.

PloS one

Monica G Risley, Stephanie P Kelly, Kailiang Jia, Brock Grill, Ken Dawson-Scully

Affiliations

  1. Department of Biological Sciences, Florida Atlantic University, Boca Raton, Florida, United States of America.
  2. Department of Neuroscience, The Scripps Research Institute, Scripps Florida, Jupiter, Florida, United States of America.

PMID: 27668426 PMCID: PMC5036823 DOI: 10.1371/journal.pone.0163786

Abstract

The microscopic nematode Caenorhabditis elegans has emerged as a valuable model for understanding the molecular and cellular basis of neurological disorders. The worm offers important physiological similarities to mammalian models such as conserved neuron morphology, ion channels, and neurotransmitters. While a wide-array of behavioral assays are available in C. elegans, an assay for electroshock/electroconvulsion remains absent. Here, we have developed a quantitative behavioral method to assess the locomotor response following electric shock in C. elegans. Electric shock impairs normal locomotion, and induces paralysis and muscle twitching; after a brief recovery period, shocked animals resume normal locomotion. We tested electric shock responses in loss-of-function mutants for unc-25, which encodes the GABA biosynthetic enzyme GAD, and unc-49, which encodes the GABAA receptor. unc-25 and unc-49 mutants have decreased inhibitory GABAergic transmission to muscles, and take significantly more time to recover normal locomotion following electric shock compared to wild-type. Importantly, increased sensitivity of unc-25 and unc-49 mutants to electric shock is rescued by treatment with antiepileptic drugs, such as retigabine. Additionally, we show that pentylenetetrazol (PTZ), a GABAA receptor antagonist and proconvulsant in mammalian and C. elegans seizure models, increases susceptibility of worms to electric shock.

Conflict of interest statement

The authors declare no conflicts of interests with one of the funding sources Eco Neurologics Inc., where the company had no role in study design, data collection and analysis, decision to publish, or

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