Abstract
The nematode Caenorhabditis elegans is a useful model organism for dissecting molecular mechanisms of neurological diseases. While hermaphrodite C. elegans contains only 302 neurons, the conserved homologous neurotransmitters, simpler neuronal circuitry, and fully mapped connectome make it an appealing model system for neurological research. Here we developed an assay to induce an electroconvulsive seizure in C. elegans which can be used as a behavioral method of analyzing potential anti-epileptic therapeutics and novel genes involved in seizure susceptibility. In this assay, worms are suspended in an aqueous solution as current is passed through the liquid. At the onset of the shock, worms will briefly paralyze and twitch, and shortly after regain normal sinusoidal locomotion. The time to locomotor recovery is used as a metric of recovery from a seizure which can be reduced or extended by incorporating drugs that alter neuronal and muscular excitability.
Keywords: Epilepsy, Seizure, C. elegans, Electroshock, Electroconvulsion, Antiepileptic drugs, AEDs
Background
We were interested in using the powerful genetic model, Caenorhabditis elegans, to develop an electroconvulsive seizure assay that can be easily manipulated by pharmacology. Invertebrate models have been used in seizures research for decades (Lee and Wu, 2002) however there were no protocols specifically investigating electroconvulsive seizures in C. elegans. In the past, multiple groups have developed methods of analyzing paralysis in response to chemical proconvulsants such as the GABAA receptor blockers, pentylentetrazol (PTZ) and picrotoxin (PTX), as well as an acetylcholinesterase inhibitor, aldicarb (Williams et al., 2004; Vashlishan et al., 2008). While these methods typically analyze the time to paralysis, our method quantifies the time it takes to recover from an electric shock-induced seizure (Risley et al., 2016).
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Acknowledgments
We have published this protocol in (Risley et al., 2016; Opperman et al., 2017). Some strains were provided by the CGC, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440).
References
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