• Hyun Young Choi, Joon Ha Park, Bai Hui Chen, Bich Na Shin, Yun Lyul Lee, In Hye Kim, Jeong-Hwi Cho, Tae-Kyeong Lee, Jae-Chul Lee, Moo-Ho Won, Ji Hyeon Ahn, Hyun-Jin Tae, Bing Chun Yan, In Koo Hwang, Jun Hwi Cho, Young-Myeong Kim, and Sung Koo Kim.
• Department of Emergency Medicine, Gangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, 07441, South Korea.
• Neurochem. Res. 2016 Sep 1; 41 (9): 2380-90.

AbstractLacosamide is a new antiepileptic drug which is widely used to treat partial-onset seizures. In this study, we examined the neuroprotective effect of lacosamide against transient ischemic damage and expressions of antioxidant enzymes such as Zn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2), catalase (CAT) and glutathione peroxidase (GPX) in the hippocampal cornu ammonis 1 (CA1) region following 5 min of transient global cerebral ischemia in gerbils. We found that pre-treatment with 25 mg/kg lacosamide protected CA1 pyramidal neurons from transient global cerebral ischemic insult using hematoxylin-eosin staining and neuronal nuclear antigen immunohistochemistry. Transient ischemia dramatically changed expressions of SOD1, SOD2 and GPX, not CAT, in the CA1 pyramidal neurons. Lacosamide pre-treatment increased expressions of CAT and GPX, not SOD1 and 2, in the CA1 pyramidal neurons compared with controls, and their expressions induced by lacosamide pre-treatment were maintained after transient cerebral ischemia. In brief, pre-treatment with lacosamide protected hippocampal CA1 pyramidal neurons from ischemic damage induced by transient global cerebral ischemia, and the lacosamide-mediated neuroprotection may be closely related to increases of CAT and GPX expressions by lacosamide pre-treatment.

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