MODULATION OF DOPAMINE D-3 RECEPTOR-BINDING BY N-ETHYLMALEIMIDE AND NEUROTENSIN

被引：23

作者：

LIU, Y ^{[1
]}

HILLEFORSBERGLUND, M ^{[1
]}

VONEULER, G ^{[1
]}

机构：

[1] KAROLINSKA INST,DEPT NEUROSCI,S-17177 STOCKHOLM,SWEDEN

来源：

BRAIN RESEARCH | 1994年 / 643卷 / 1-2期

关键词：

DOPAMINE RECEPTOR; 7-[H-3]HYDROXY-N; N-DI-N-PROPYL-2-AMINOTETRALIN; G PROTEIN; RACLOPRIDE; REMOXIPRIDE; N-PROPYLNORAPOMORPHINE; QUINPIROLE; MAGNESIUM;

D O I：

10.1016/0006-8993(94)90045-0

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

GTP or G protein inactivation by N-ethylmaleimide reduced the B-max value but not the K-D value of 7-[H-3]hydroxy-N,N-di-n-propyl-2-aminotetralin ([H-3]7-OH-DPAT) binding in the rat subcortical limbic area. Neurotensin (10 nM) increased the K-D and the B-max values of [3H]7-OH-DPAT binding, and these effects persisted also following N-ethylmaleimide pretreatment. N-Propylnorapomorphine, quinpirole, raclopride, and remoxipride inhibited [H-3]7-OH-DPAT binding with K-i values of 0.093, 1.97, 10.6, and 710 nM, respectively. These findings indicate that the D-3 receptor is coupled to G proteins in the brain, and that neurotensin can modulate D-3 agonist binding by a G protein-independent mechanism.

引用

页码：343 / 348

页数：6

共 23 条

[1] NEUROTENSIN INVITRO MARKEDLY REDUCES THE AFFINITY IN SUBCORTICAL LIMBIC N-PROPYLNORAPOMORPHINE-H-3 BINDING-SITES [J].