Pan J C, Pei Y Q, An L, Lai L
Department of Pharmacology, Beijing Medical University.
Yao Xue Xue Bao. 1996;31(8):561-7.
Intrahippocampal injection(ihci) of guanidinosuccinic acid (GSA) to rats, induced typical generarized clonic seizures and epileptiform discharges in electrohippocampogram (EHG) and electrocorticogram (ECoG), degenerative changes of neuronal cells in the injected side hippocampus. The pyramidal cells in CA1 area were found to be more vulnerable to GSA than the granular cells. Phenobarbital and phenytoin are typical antiepiletics, but in no case did they successfully protect against GSA induced convulsions, epileptiform discharges in the EHG and ECoG and neurolysis. Ketamine, a selective noncompetitive NMDA receptor antagonist, was shown to protect against not only seizures, but also neuronal cell damage induced by GSA. All these results indicate that GSA very like the endogenous excitatory amino acid, glutamic acid, it also has such effects mentioned above. Therefore, the NMDA receptor may mediate both effects of GSA.
向大鼠海马内注射胍基琥珀酸（GSA），可诱发典型的全身性阵挛性惊厥以及脑电图（EHG）和皮质电图（ECoG）中的癫痫样放电，注射侧海马的神经元细胞发生退行性变化。发现CA1区的锥体细胞比颗粒细胞更容易受到GSA的影响。苯巴比妥和苯妥英是典型的抗癫痫药，但它们均未能成功预防GSA诱发的惊厥、EHG和ECoG中的癫痫样放电以及神经溶解。氯胺酮是一种选择性非竞争性NMDA受体拮抗剂，已证明它不仅可以预防癫痫发作，还可以预防GSA诱导的神经元细胞损伤。所有这些结果表明，GSA非常类似于内源性兴奋性氨基酸谷氨酸，它也具有上述作用。因此，NMDA受体可能介导了GSA的两种作用。
