Abstract
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.
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