Outward currents in voltage‐clamped rat sympathetic neurones.
- 1 November 1984
- journal article
- research article
- Published by Wiley in The Journal of Physiology
- Vol. 356 (1), 115-133
- https://doi.org/10.1113/jphysiol.1984.sp015456
Abstract
Outward membrane currents were studied in neurons of the isolated rat superior cervical ganglion by using a 2-microelectrode or single-microelectrode voltage-clamp technique. Under current clamp, depolarization elicited electrotonic potentials that displayed marked outward rectification. From negative resting potentials (-70 mV) a short latency, short duration outward rectification was observed. From more positive potentials (-40 mV) a longer latency persistent outward rectification could be demonstrated. Under voltage clamp, 4 distinct outward currents were observed: a delayed rectifier (IK); a transient outward current (IA); a Ca2+-activated content (IC) and the M-current (IM). The maximum amplitude of IK, IA and IC was 1-2 orders of magnitude greater than IM. Depolarizing from -40 mV to potentials more positive than -20 mV coactivated IK and IC, producing a characteristic N-shaped current voltage curve with a minimum at about +80 mV. Superfusion with Mn2+-containing solutions reduced outward current at all voltages and abolished the N-characteristic; the remaining current (IK) slowly inactivated (.tau. > 1 s). Raising [K+]o from 6 to 36 mmol/l reversed outward tail currents observed in normal solution. Addition of tetraethylammonium ions (1-3 mmol/l) strongly reduced the amplitude of IK and IC. IA was characterized by very rapid activation at potentials more positive than -60 mV and by fast and complete inactivation at potentials in the activation range. The amplitude of IA was dependent on [K+]o and was reduced by external 4-aminopyridine (1-3 mmol/l). The activation appeared to depend on the nature and concentration of divalent cations present in the superfusate. The soma membrane of rat sympathetic neurons, like many other vertebrate and invertebrate neurons, contains multiple populations of K+ channels. The possible functions of these in the control of ganglion cell excitability are discussed.This publication has 21 references indexed in Scilit:
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