INTRACELLULAR techniques were used to study the actions of dopaminergi
c D-1 agonists on the afterhyperpolarization (AHP) that follows action
potentials in rat neostriatal neurones. Dopamine or Cl-APB (10 mu M),
or 1-10 mu M 6-Cl-PB all increased AHP amplitude. This effect was blo
cked by 1 mu M SCH-23390, a D-1 antagonist, but not by 1 mu M sulpirid
e, a D-2 antagonist. Both 500 mu M dibutyryl cAMP and 5 mu M Bay K 864
4 induced a similar AHP increase. Bay K 8644 occluded the effect of ag
onists. The results suggest that the action of dopamine is mediated vi
a the recently described protein kinase A enhancement of L-type Ca2+ c
hannels. The results partially explain the decrease in firing frequenc
y induced by dopamine and a possible site of antagonism with cholinerg
ic modulation.