Zapata A, Capdevila J L, Viu E, Trullas R
Unitat de Neurobiologia, CID, CSIC, Barcelona, Spain.
Neuroreport. 1996 Jan 31;7(2):397-400. doi: 10.1097/00001756-199601310-00005.
The effect of systemic treatment with 1-aminocyclopro-panecarboxylic acid (ACPC), a partial agonist at the glycine site of the NMDA receptor, on convulsions and neurodegeneration induced by intrahippocampal injection of NMDA was investigated in mice. Five days after intrahippocampal NMDA infusion, 80-100% pyramidal cell death was observed in the CA1 region of the hippocampus. Pretreatment with ACPC prevented the lethal effects of NMDA and significantly reduced seizure induction. ACPC reduced cell death to 40% of that induced by a dose of NMDA (6 nmol) that damaged 80% of hippocampal CA1 neurones in untreated animals. These findings provide further evidence that ACPC can reduce NMDA receptor function in vivo and suggest that partial agonists at the glycine site of the NMDA receptor complex may be useful anticonvulsant and neuroprotective agents.
在小鼠中研究了用1-氨基环丙烷羧酸（ACPC）进行全身治疗的效果，ACPC是N-甲基-D-天冬氨酸（NMDA）受体甘氨酸位点的部分激动剂，其对海马内注射NMDA诱导的惊厥和神经退行性变的影响。海马内注入NMDA五天后，在海马CA1区观察到80-100%的锥体细胞死亡。ACPC预处理可预防NMDA的致死作用，并显著降低癫痫发作的诱导。ACPC将细胞死亡减少至未治疗动物中由6 nmol剂量的NMDA诱导的细胞死亡的40%，该剂量的NMDA可损伤80%的海马CA1神经元。这些发现提供了进一步的证据，表明ACPC可在体内降低NMDA受体功能，并提示NMDA受体复合物甘氨酸位点的部分激动剂可能是有用的抗惊厥和神经保护剂。
