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首页> 美国政府科技报告 >NMDA (N-Methyl-D-Aspartate)-Receptor Antagonist, MK-801, Suppresses Limbic Kindling and Kindled Seizures
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NMDA (N-Methyl-D-Aspartate)-Receptor Antagonist, MK-801, Suppresses Limbic Kindling and Kindled Seizures

机译：NmDa（N-甲基-D-天冬氨酸） - 受体拮抗剂，mK-801，抑制边缘点燃和点燃癫痫发作

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The role of excitatory amino acid neurotransmission in electrical kindling was examined in animals stimulated daily in the amygdala following ip administration of low dosages of MK-801 (0.1 and 0.5 mg/kg). A second experiment evaluated the anticonvulsant properties of MK-801 in rats kindled in the hippocampus and amygdala, and contrasted its efficacy with the antiepileptic agents diazepam, phenobarbital and phenytoin, and the dissociative anesthetics phencyclidine and ketamine. MK-801 (0.5 mg/kg) retarded the development of amygdala kindling and reduced mean afterdischarge (AD) duration over the first 10 stimulation sessions. The low dosage reduced total AD accrued during each kindling stage but failed to alter kindling rate. MK-801 blocked motor seizures induced by stimulation of hippocampal or amygdala kindled foci, but was more effective in reducing seizure severity and AD duration resulting from stimulation of the hippocampal focus. All other drugs tested, with the exception of phenytoin, protected against amygdaloid kindled seizures. It was concluded that excitatory amino acid transmission contributes in an important, but noncritical way to amygdala kindling. (Copyright (c) 1988 Elsevier Science Publishers B.V. (Biomedical Division).)

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