金刚烷胺可诱导大鼠纹状体中的c-fos：多巴胺D1受体拮抗剂和N-甲基-D-天冬氨酸受体拮抗剂可使其逆转。

Amantadine induces c-fos in rat striatum: reversal with dopamine D1 and NMDA receptor antagonists.

作者信息

Tomitaka S, Hashimoto K, Narita N, Minabe Y, Tamura A

机构信息

Department of Cortical Function Disorder, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.

出版信息

Eur J Pharmacol. 1995 Oct 16;285(2):207-11. doi: 10.1016/0014-2999(95)00504-e.

DOI:10.1016/0014-2999(95)00504-e

PMID:8566141

Abstract

Amantadine (1-aminoadamantane) induced Fos expression in the central, dorsal-medial and ventral-medial part of the striatum. The distribution pattern of Fos induced by amantadine was more similar to those seen with dopaminomimetics than with N-methyl-D-aspartate (NMDA) receptor antagonists. Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the NMDA receptor antagonist, MK-801, blocked amantadine induction of Fos in the striatum. However, amantadine induction of Fos in the striatum was unaffected by the dopamine D2 receptor antagonist, sulpiride. These results suggest that amantadine induction of Fos in the rat striatum is related to dopamine D1 and NMDA receptors.

摘要

金刚烷胺（1-氨基金刚烷）可诱导纹状体中央、背内侧和腹内侧部分出现Fos表达。金刚烷胺诱导的Fos分布模式与多巴胺模拟物诱导的模式比与N-甲基-D-天冬氨酸（NMDA）受体拮抗剂诱导的模式更为相似。用多巴胺D1受体拮抗剂SCH23390和NMDA受体拮抗剂MK-801进行预处理，可阻断金刚烷胺诱导纹状体中Fos的产生。然而，多巴胺D2受体拮抗剂舒必利对金刚烷胺诱导纹状体中Fos的产生没有影响。这些结果表明，金刚烷胺诱导大鼠纹状体中Fos的产生与多巴胺D1和NMDA受体有关。