E-ISSN: 1019-5157
ISSN: 2651-5024
Research
Evaluation of Group 1 Metabotropic Glutamate Receptors Expression After Lacosamide Treatment in a Kainic Acid–Induced Temporal Lobe Epilepsy Model
Fırat Narin✉ ,
Turak Rehimli ,
Şahin Hanalıoğlu ,
Zarifa Yusifli ,
Hıdır Ozer ,
İbrahim Başar ,
Alaeddin Acar ,
Mustafa Berker
Neurosurgery, Mersin City Hospital; Department of Neurosurgery, HACETTEPE UNIVERSITY; Department of Neurosurgery, Ordu University, Faculty of Medicine; Neurosurgery, Kulu State Hospital
DOI: 10.5137/1019-5149.JTN.50380-26.3
Accepted: 28/06/2026
Article in Press
Corresponding Author:
Fırat Narin (drfiratnarin@gmail.com)
Abstract
Aim
The present study aimed to investigate the effects of lacosamide (LCM), an antiepileptic agent, on the expression of group 1 metabotropic glutamate receptors (mGluR1 and mGluR5) in a temporal lobe epilepsy (TLE) model.
Material and Methods
Thirty-two rats were divided into four groups defined by the following treatments: (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 kainic acid injection, and intraperitoneal LCM administration (50 mg/kg/day) for 2 weeks.
Results
No hippocampal sclerosis was detected in group 2, but sclerosis was observed in groups 3 and 4. Although mGluR1 and mGluR5 expression was increased on the side of kainic acid injection, LCM exerted no significant effect on the expression of these receptors.
Conclusion
The antiepileptic effect of LCM is likely not mediated through group I metabotropic glutamate receptors. Since the efficacy of mGluR1 and mGluR5 antagonist monotherapy in drug-resistant TLE remains uncertain, these findings suggest that LCM may act through alternative mechanisms warranting further investigation.
The present study aimed to investigate the effects of lacosamide (LCM), an antiepileptic agent, on the expression of group 1 metabotropic glutamate receptors (mGluR1 and mGluR5) in a temporal lobe epilepsy (TLE) model.
Material and Methods
Thirty-two rats were divided into four groups defined by the following treatments: (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 kainic acid injection, and intraperitoneal LCM administration (50 mg/kg/day) for 2 weeks.
Results
No hippocampal sclerosis was detected in group 2, but sclerosis was observed in groups 3 and 4. Although mGluR1 and mGluR5 expression was increased on the side of kainic acid injection, LCM exerted no significant effect on the expression of these receptors.
Conclusion
The antiepileptic effect of LCM is likely not mediated through group I metabotropic glutamate receptors. Since the efficacy of mGluR1 and mGluR5 antagonist monotherapy in drug-resistant TLE remains uncertain, these findings suggest that LCM may act through alternative mechanisms warranting further investigation.
Keywords
Kainic acid
lacosamide
temporal lobe epilepsy
hippocampal sclerosis
glutamate receptor