Evaluation of Group 1 Metabotropic Glutamate Receptors Expression After Lacosamide Treatment in a Kainic Acid-Induced Temporal Lobe Epilepsy Model.

AIM: To investigate the effects of lacosamide (LCM), an antiepileptic agent, on group 1 metabotropic glutamate receptors (mGluR1 and mGluR5) expression in a temporal lobe epilepsy (TLE) model. MATERIAL and

METHODS

Thirty-two rats were divided into 4 groups: (1) only burr hole without intrahippocampal injection, (2) burr hole and stereotaxic intrahippocampal saline injection, (3) burr hole, stereotaxic intrahippocampal kainic acid injection and 2 weeks of intraperitoneal saline treatment, and (4) burr hole, stereotaxic intrahippocampal KA injection and 50mg/kg intraperitoneal LCM treatment for 2 weeks.

RESULTS

No hippocampal sclerosis was detected in group 2 but sclerosis was observed in Groups 3 and 4. Despite increase in mGluR1 and mGluR5 expressions on the side of kainic acid injection, no significant effect of LCM was found on mGluR1 or mGluR5 expression. In the experimental rat model of TLE with intrahippocampal kainic acid injection in the present study, LCM was found to have no effect on mGluR expression in Group 1.

CONCLUSION

The antiepileptic effect of LCM does not seem to be mediated through group I metabotropic glutamate receptors. Since the efficacy of mGluR1 and mGluR5 antagonists as monotherapy in drug-resistant TLE remains uncertain, these findings suggest that lacosamide may act through alternative mechanisms, which require further investigation.