Abstracts

Rationale: Temporal lobe epilepsy (TLE) is one of the principal causes of cognitive impairment that may be followed by brain injury after seizure. When the brain was injured after seizure, free zinc can be released from presynaptic terminals and then translocated into intracellular space and accumulated. Excessive accumulation of intracellular free zinc initiates neuronal death after seizure. Transient receptor potential melastatin 7 (TRPM7) channel is known as a channel that specifically participates in the transport of zinc. Carvacrol is an essential oil extracted from Origanum vulgare, which acts as a TRPM7 channel inhibitor. So, we hypothesized that carvacrol may have a neuroprotective effect by reducing excessive zinc translocation after seizure.   Methods: TLE was induced by lithium-pilocarpine in male rats. We injected lithium chloride (125mg/kg, i.p.) at 19 hour before administration of pilocarpine. And then we injected scopolamine (2mg/kg, i.p.) at 30 minutes before pilocarpine injection. After inject pilocarpine (25mg/kg, i.p.), we performed behavioral test based on Racine stage. Carvacrol (50mg/kg/day, i.p.) was injected every day for 3 days after pilocarpine injection. To detect of degenerating neurons, oxidative injury, microglia activation and TRPM7 channel activation, we performed Fluoro-Jade B, 4HNE, Iba1, and TPRM7 staining, respectively. We also performed TSQ staining to determine the level of free zinc accumulation in the neuron.  Results: The present study demonstrates that carvacrol reduced the number of degenerating neurons, oxidative injury, microglia activation, TRPM7 channel activation and zinc accumulation after seizure.  Conclusions: Therefore, the present study suggests that carvacrol that inhibits TRPM7 channel has neuroprotective effects by reducing the abnormal translocation of free zinc in the neuron after seizure.  Funding: No funding