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增强培养的哺乳动物脊髓神经元中γ-氨基丁酸介导的突触后抑制:一种常见的抗惊厥作用模式。

Enhancement of GABA-mediated postsynaptic inhibition in cultured mammalian spinal cord neurons: a common mode of anticonvulsant action.

作者信息

MacDonald R L, Barker J L

出版信息

Brain Res. 1979 May 11;167(2):323-36. doi: 10.1016/0006-8993(79)90826-6.

Abstract

Murine spinal cord neurons grown in dissociated cell culture were used to study the effects of barbiturate (phenobarbital, mephobarbital) and benzodiazepine (diazepam, chlordiazepoxide( anticonvulsants on amino acid responses. Both types of anticonvulsant augmented GABA-mediated postsynaptic inhibition without augmenting beta-alanine or glycine-mediated postsynaptic inhibition. Barbiturates, but not benzodiazepines, antagonized glutamate-mediated postsynaptic excitation. Augmentation of GABA-mediated inhibition by the anticonvulsants should contribute to their anticonvulsant action; antagonism of glutamate-mediated excitation by barbiturates should also contribute to their anticonvulsant action and could be at least in part responsible for their sedative actions.

摘要

在解离细胞培养中生长的小鼠脊髓神经元被用于研究巴比妥类药物(苯巴比妥、美索比妥)和苯二氮䓬类药物(地西泮、氯氮䓬)这两种抗惊厥药对氨基酸反应的影响。两种类型的抗惊厥药都增强了γ-氨基丁酸(GABA)介导的突触后抑制,而没有增强β-丙氨酸或甘氨酸介导的突触后抑制。巴比妥类药物而非苯二氮䓬类药物拮抗了谷氨酸介导的突触后兴奋。抗惊厥药增强GABA介导的抑制作用应有助于其抗惊厥作用;巴比妥类药物对谷氨酸介导的兴奋的拮抗作用也应有助于其抗惊厥作用,并且可能至少部分地导致其镇静作用。

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