Quinine blocks a calcium-activated potassium conductance in mammalian enteric neurones.
Quinine (100 microM) abolished the slow calcium-dependent afterhyperpolarization which occurs after an action potential in some neurones of the guinea-pig myenteric and submucous plexus. This occurred without any effect on the amplitude or time course of the action potential itself, or on the faster calcium-independent afterhyperpolarization. Tetraethylammonium did not reduce the slow afterhyperpolarization. Quinine also abolished the hyperpolarization which was evoked by intracellular injection of calcium ions.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000037:antagonists & inhibitors* / Q000502:physiology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007422:Intestines / Q000294:innervation*; D007473:Ion Channels / Q000187:drug effects*; D009197:Myenteric Plexus / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D011803:Quinine / Q000494:pharmacology*; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D007473:Ion Channels; D013757:Tetraethylammonium Compounds; D011803:Quinine; D011188:Potassium; D002118:Calcium