Hyperpolarization following activation of K+ channels by excitatory postsynaptic potentials.
We have postulated that an excitatory postsynaptic potential (e.p.s.p.) may open voltage-sensitive K+ ('M') channels, in an appropriate depolarizing range, and that this could alter the e.p.s.p. waveform. Consequently, the fast e.p.s.p. in neurones of sympathetic ganglia, elicited by a nicotinic action of acetylcholine (ACh), could be followed by a hyperpolarization, produced by the opening of M channels during the depolarizing e.p.s.p. and their subsequent slow closure (time constant-150 mg). This introduces the concept that transmitter-induced p.s.ps may trigger voltage-sensitive conductances other than those initiating action potentials, and that in the present case this could produce a true post-e.p.s.p. hyperpolarization. (Some hyperpolarizations other than inhibitory postsynaptic potentials (i.p.s.ps) have been reported to follow e.p.s.ps.) We show here that this is so.
D000818:Animals; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D008564:Membrane Potentials; D009116:Muscarine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D011892:Rana catesbeiana; D013569:Synapses / Q000502:physiology*; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D007473:Ion Channels; D013757:Tetraethylammonium Compounds; D009116:Muscarine; D011188:Potassium