纹状体的 kainic 酸损伤会增加多巴胺释放，但会降低 3-甲氧基酪胺水平。

Kainic acid lesion of the striatum increases dopamine release but reduces 3-methoxytyramine level.

作者信息

Naudon L, Dourmap N, Leroux-Nicollet I, Costentin J

机构信息

Unité de Neuropsychopharmacologie Expérimentale, U.R.A. 1170 du CNRS, Faculté de Médecine et de Pharmacie de Rouen, Saint Etienne du Rouvray, France.

出版信息

Brain Res. 1992 Feb 14;572(1-2):247-9. doi: 10.1016/0006-8993(92)90477-q.

DOI:10.1016/0006-8993(92)90477-q

PMID:1611519

Abstract

Kainic acid lesion of the striatum leads to the disruption of the striatonigral regulatory loop. Although microdialysis showed an increase in dopamine release, two days after kainic acid injection, 3-methoxytyramine levels are dramatically decreased. This suggests that the postsynaptic membrane-bound catechol-O-methyltransferase (COMT), but not the glial COMT, is responsible for the formation of measured 3-methoxytyramine.

摘要

纹状体的 kainic 酸损伤导致纹状体黑质调节环路的破坏。尽管微透析显示多巴胺释放增加，但在注射 kainic 酸两天后，3-甲氧基酪胺水平显著降低。这表明，测得的 3-甲氧基酪胺的形成是由突触后膜结合儿茶酚-O-甲基转移酶（COMT）而非胶质 COMT 负责。