Nicotine inhibits slowly inactivating K+ currents in rat cultured striatal neurons.
As shown on cultured striatal neurons recorded in whole-cell configuration, both acetylcholine (in the presence of atropine) and nicotine reduced voltage-dependent outward currents. Although, at early postnatal ages, outward currents in these cells are mainly carried by rapidly and slowly inactivating K+ channels, these inhibitions resulted from a selective and reversible effect on the slowly inactivating K+ conductance (IK+). This action was blocked by the nicotinic antagonist dihydro-beta-erythroïdine and reproduced by nicotinic agonists. When neurons were recorded under current-clamp conditions, nicotine increased reversibly their firing rate generated by step depolarizations. Therefore, in addition to its well documented muscarinic effects, acetylcholine also controls K+ currents in striatal neurons through mechanisms mediated by nicotinic receptors.
Hamon
B
B
INSERM U114, Collège de France, Paris, France.
Glowinski
J
J
Giaume
C
C
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002478:Cells, Cultured; D003342:Corpus Striatum / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004079:Dihydro-beta-Erythroidine / Q000494:pharmacology; D004553:Electric Conductivity; D009474:Neurons / Q000187:drug effects* / Q000502:physiology*; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D011188:Potassium / Q000037:antagonists & inhibitors* / Q000502:physiology*; D051381:Rats / Q000196:embryology; D017207:Rats, Sprague-Dawley
D018722:Nicotinic Agonists; D018733:Nicotinic Antagonists; D004079:Dihydro-beta-Erythroidine; D009538:Nicotine; D000109:Acetylcholine; D011188:Potassium