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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / pharmacology
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Action Potentials / drug effects
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Action Potentials / physiology
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Animals
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Bucladesine / pharmacology
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Calcium Channel Agonists / pharmacology
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Dopamine / pharmacology
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Dopamine / physiology*
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Dopamine D2 Receptor Antagonists
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In Vitro Techniques
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Neostriatum / cytology
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Neostriatum / drug effects
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Neostriatum / physiology*
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Neurons / drug effects
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Neurons / physiology*
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Rats
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Receptors, Dopamine D1 / agonists
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Receptors, Dopamine D1 / antagonists & inhibitors
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Receptors, Dopamine D2 / agonists
Substances
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Calcium Channel Agonists
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Dopamine D2 Receptor Antagonists
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Receptors, Dopamine D1
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Receptors, Dopamine D2
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Bucladesine
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3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
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Dopamine