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Effects of Lamotrigine on brain nitrite and cGMP levels during focal cerebral ischemia in rats
Author(s) -
Balkan S.,
Özben T.,
Balkan E.,
Oguz N.,
Serteser M.,
Gümüslü S.
Publication year - 1997
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1997.tb00085.x
Subject(s) - lamotrigine , ischemia , glutamate receptor , nmda receptor , neurotoxicity , anesthesia , glutamatergic , anticonvulsant , nitric oxide , pharmacology , medicine , epilepsy , receptor , toxicity , psychiatry
Glutamate receptor antagonists are protective in animal models of focal cerebral ischemia. Lamotrigine (3,5‐diamino‐6‐[2,3‐dichlorophenyl]‐1,2,4‐triazine) is an anticonvulsant drug that blocks voltage‐gated sodium channels and inhibits the ischemia‐induced release of glutamate. Experiments in primary neuronal cultures implicate nitric oxide (NO) as a mediator of glutamatergic neurotoxicity acting via N‐Methyl‐ d ‐Aspartate (NMDA) receptors. The effect of glutamate release inhibitor, Lamotrigine upon NO and cGMP production has been examined in focal cerebral ischemia in rats. Focal cerebral ischemia was produced by the permanent occlusion of right middle cerebral artery (MCA) in urethane anesthetized rats. A number of indicators of brain NO production (nitrite, cGMP) were determined in ipsilateral and contralateral cerebral cortex and cerebellum after 0, 10, 60 min of focal cerebral ischemia. The same parameters were measured in rats treated with Lamotrigine (20 mg/kg, i.p.) 30 min before or just after the occlusion of the right MCA.