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.
Highlights
Caenorhabditis elegans has begun to emerge as a powerful in vivo model for research on neurological conditions including neurodegenerative diseases and neurodevelopmental disorders [1,2,3,4,5,6,7]
Our results indicate that immediately following a brief threesecond electric shock, young adult worms exhibit paralysis with body stiffness and elongation
We have shown that GABAergic neurotransmission plays a role in the time to recovery after electric shock, and that recovery time can be decreased by treatment with antiepileptics and increased with PTZ
Summary
Caenorhabditis elegans has begun to emerge as a powerful in vivo model for research on neurological conditions including neurodegenerative diseases and neurodevelopmental disorders [1,2,3,4,5,6,7]. C. elegans possesses a relatively simple nervous system, but has important conserved features of nervous system function at the level of ion channels and neurotransmitters. Of particular relevance to this study is the conservation of gamma-aminobutyric acid (GABA) and GABA receptors in inhibitory neurotransmission, and acetylcholine. C. elegans Electroshock Assay analysis, decision to publish, or preparation of the manuscript. This funding does not alter our adherence to PLOS ONE policies on sharing data and materials. (ACh) and acetylcholine receptors in excitatory neurotransmission [8,9,10,11]. In addition to physiological similarities, C. elegans has a fully mapped connectome, is small and inexpensive to maintain and preserve, has a short three-day generation time, and is conducive for large-scale screening [12,13,14,15,16,17]
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