Liao J X, Wang L, Zuo C H
Department of Pediatrics, First Hospital of Beijing Medical University 100034.
Yao Xue Xue Bao. 1997;32(2):137-9.
Mechanisms underlying tolerance to and dependence on the anticonvulsant effect of clonazepam are not clear. Autoradiography of the NMDA receptors in amygdala-kindled rats with tolerance to and dependence on the anticonvulsant effect of clonazepam was carried out. When tolerance developed, the binding of [3H] TCP (N-(1-thieny) cyclohexylpiperidine) to NMDA receptors was found to be increased at the polymorphocellular layer of the right CA1, and decreased at the molecular layer of the cerebellar ansiform lobule. On day 7 of the discontinuation of clonazepam, the binding did not change further. These changes may be responsible for the tolerance to and dependence on the anticonvulsant effect of clonazepam. However, the exact significance of these results should be further investigated.
氯硝西泮抗惊厥作用的耐受和依赖机制尚不清楚。对氯硝西泮抗惊厥作用产生耐受和依赖的杏仁核点燃大鼠进行了NMDA受体的放射自显影研究。当产生耐受时,发现[3H]TCP(N-(1-噻吩基)环己基哌啶)与NMDA受体的结合在右侧CA1的多形细胞层增加,而在小脑袢叶的分子层减少。在停用氯硝西泮的第7天,结合没有进一步变化。这些变化可能是对氯硝西泮抗惊厥作用产生耐受和依赖的原因。然而,这些结果的确切意义仍需进一步研究。