NICOTINE INHIBITS SLOWLY INACTIVATING K+ CURRENTS IN RAT CULTURED STRIATAL NEURONS

As shown on cultured striatal neurons recorded in whole-cell configura tion, both acetylcholine (in the presence of atropine) and nicotine re duced voltage-dependent outward currents. Although, at early postnatal ages, outward currents in these cells are mainly carried by rapidly a nd slowly inactivating K+ channels, these inhibitions resulted from a selective and reversible effect on the slowly inactivating K+ conducta nce (I-K+). This action was blocked by the nicotinic antagonist dihydr o-beta-erythroidine and reproduced by nicotinic agonists. When neurons were recorded under current-clamp conditions, nicotine increased reve rsibly 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 media ted by nicotinic receptors.