Hernández-López S, Bargas J, Reyes A, Galarraga E
Departamento de Neurociencias, UNAM, México City, DF, México.
Neuroreport. 1996 Jan 31;7(2):454-6. doi: 10.1097/00001756-199601310-00019.
Intracellular techniques were used to study the actions of dopaminergic D1 agonists on the afterhyperpolarization (AHP) that follows action potentials in rat neostriatal neurones. Dopamine or Cl-APB (10 microM), or 1-10 microM 6-Cl-PB all increased AHP amplitude. This effect was blocked by 1 microM SCH-23390, a D1 antagonist, but not by 1 microM sulpiride, a D2 antagonist. Both 500 microM dibutyryl cAMP and 5 microM BayK 8644 induced a similar AHP increase. BayK 8644 occluded the effect of agonists. The results suggest that the action of dopamine is mediated via the recently described protein kinase A enhancement of L-type Ca2+ channels. The results partially explain the decrease in firing frequency induced by dopamine and a possible site of antagonism with cholinergic modulation.
采用细胞内技术研究多巴胺能D1激动剂对大鼠新纹状体神经元动作电位后超极化(AHP)的作用。多巴胺或Cl-APB(10微摩尔),以及1 - 10微摩尔的6-Cl-PB均可增加AHP幅度。这种效应被D1拮抗剂1微摩尔SCH-23390阻断,但不被D2拮抗剂1微摩尔舒必利阻断。500微摩尔二丁酰环磷腺苷和5微摩尔BayK 8644均可诱导类似的AHP增加。BayK 8644可阻断激动剂的作用。结果表明,多巴胺的作用是通过最近描述的蛋白激酶A增强L型钙通道来介导的。这些结果部分解释了多巴胺诱导的放电频率降低以及与胆碱能调制可能的拮抗位点。