Electroshock Summary

Electroshock is one of the most common protocols to analyze seizures in mammals and fruit flies. The authors created a new assay to assess the response of C. elegans to electroshock. Despite having a simpler nervous system, C. elegans are a commonly used in vivo model because of similar morphologies to mammals especially in GABA inhibitory neurotransmission. Other convulsive models in C. elegans use the GABA receptor antagonist pentylenetetrazole (PTZ) to induce seizures but this compound often leads to paralysis. This novel electroshock technique is able to quantify both the paralysis and convulsions occurring in C. elegans following electric shock.
The authors started by observing the behavioral response C. elegans had to electric shock.
The results immediately showed the worms paralyzed and elongated during a 3 second shock which was followed by convulsions. Upon cessation of the electric current the worms rapidly recovered their normal swimming pattern. This swimming movement, simply, is caused by excitatory cholinergic transmission on one side of the body while the other side uses GABAergic transmission to relax the muscles on the opposite. The authors proceeded to ask whether alterations in GABA neurotransmission would alter the recovery time in these C. elegans. A mutant worm, unc-25, unable to synthesize GABA, was subjected to the new electroshock protocol. The observations indicate that unc-25 worms had a slower recovery time than the wildtype, 89.5 +/- 105 seconds and 33.45 +/- 4.5 seconds respectively. The authors believe this reduction in recovery time implies that a loss of GABAergic transmissions causes and increased sensitivity to electric shock. To confirm this, the group used several antiepileptic drugs to observe their effects on the recovery time. Though the recovery time in wild-type worms was not affected, in the unc-25 worms the results show a quicker recovery. To further validate the protocol, wild-type C. elegans were treated with PTZ and then challenged with one of the antiepileptic drugs, RTG, used earlier. The results show that 72mM PTZ
elegans. Although this study is well designed and potential shortcomings were elaborated on, there was one major discrepancy that was not addressed involving the unc-25 worms and PTZ treatment. In the discussion, the authors explain that unc-25 did not survive incubation in PTZ at 72mM and suggest this may be due to discrepancies in the knockout status of unc-25 or PTZ inhibiting calcium channels in addition to GABA signaling. Though the result section indicated that unc-25 did not survive, these worms were subjected to electroshock for roughly 6 minutes. This presents a question on whether the lack of recover was caused by PTZ incubation or the prolonged electrocution. They then claim that unc-25 worms were able to recover when co-treated with RTG but these worms were only exposed to electric shock for 1.5 minutes. Since this was done to assess the effect of GABA transmission on recovery, the large difference in time hinders the assumption that co-treatment with an antiepileptic can enhance the recovery