A review on drugs and toxins affecting presynaptic K+ currents and phasic quantal transmitter release at motor nerve terminals.
This review assembles available information concerning drugs and toxins which block the different types of presynaptic K+ currents and discusses the relative importance of these currents in controlling phasic quantal transmitter release. Drugs and toxins which block the fast voltage-dependent potassium current (IKf), enhance phasic acetylcholine release evoked by nerve impulses. This effect is due to increased Ca2+ influx during prolonged presynaptic membrane depolarization. Selective blockade of the Ca(2+)-dependent K+ current (IK(Ca)) does not induce any change in phasic transmitter release indicating that, under physiological conditions, IK(Ca) has no significant role in presynaptic membrane repolarization. The contribution of the slow voltage-dependent K+ current (IKs) to the regulation of phasic acetylcholine release remains to be clarified. In conclusion, IKf, IK(Ca) and IKs can modulate the entry of Ca2+ into motor nerve terminals. However, under physiological conditions only IKf plays a key role in controlling the transient Ca2+ influx which is responsible for the phasic transmitter release.
Molgó
J
J
Laboratoire de Neurobiologie Cellulaire et Moléculaire du C.N.R.S., Gif sur Yvette, France.
Tabti
N
N
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D009411:Nerve Endings / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects*
D015221:Potassium Channels; D002118:Calcium