Short communicationEffects of eugenol on granule cell dispersion in a mouse model of temporal lobe epilepsy

- We examined the inhibitory effect of EUG on GCD following KA-induced seizure.
- EUG treatment significantly reduced the development of GCD in KA-treated hippocampus.
- EUG significantly suppressed KA-induced mTORC1 activation in the hippocampal DG.
- Similar to the effect of EUG, mTORC1 deactivation by RA decreased KA-induced GCD.
- EUG may be beneficial for decreasing epileptic seizures in vivo.

Granule cell dispersion (GCD), a structural abnormality, is characteristic of temporal lobe epilepsy (TLE). Eugenol (EUG) is an essential component of medicinal herbs and is suggested to exert anticonvulsant activity. However, it is unclear whether EUG ameliorates the abnormal morphological changes in granule cells induced by epileptic insults. In the present study, we examined whether intraperitoneal injection of EUG attenuated increased seizure activity and GCD following intrahippocampal injection of kainic acid (KA). Our results showed that EUG significantly increased the seizure threshold, resulting in delayed seizure onset, and reduced GCD in KA-induced epilepsy. Moreover, EUG treatment significantly attenuated KA-induced activation of mammalian target of rapamycin complex 1 (mTORC1), which is involved in GCD development, in the dentate gyrus (DG). These results suggest that EUG may have beneficial effects in the treatment of epilepsy through its ability to inhibit GCD via suppression of KA-induced mTORC1 activation in the hippocampal DG in vivo.