Membrane‐potential effects on an inhibitory post‐synaptic conductance in Aplysia buccal ganglia.
Open Access
- 1 July 1980
- journal article
- research article
- Published by Wiley in The Journal of Physiology
- Vol. 304 (1) , 165-180
- https://doi.org/10.1113/jphysiol.1980.sp013317
Abstract
1. Inhibitory post‐synaptic currents (i.p.s.c.s) were recorded under voltage clamp using two electrodes placed in neuronal somas of the buccal ganglia of Aplysia, in order to study the effects of membrane potential (Vm) on decay time constant (tau). 2. From ‐175 to ‐40 mV, tau did not vary with Vm. At Vm more depolarized than ‐40 mV, tau decreased. Also at depolarized Vm, cell input resistance (Rin) decreased and many cells showed non‐exponential i.p.s.c. decay, including undershoot. These results suggest that the apparently faster tau is an artifact of remote membrane poorly clamped at the low Rin of depolarized levels, rather than a Vm‐dependent i.p.s.c. relaxation. 3. Injected current pulses produced voltage relaxations which decayed faster including undershoot, when Vm was depolarized beyond ‐40 mV. 4. Step commands across the reversal potential were delivered during i.p.s.c.s. Currents reversed direction, relaxing consistent with the new Vm, thus showing that recorded current decay repressants the true time course of i.p.s.c. relaxation, rather than uncontrolled slow axonal charging from a fast remote synaptic current. 5. I conclude that clamp control is poor at depolarized Vm, due to decreased Rin, and the faster, non‐exponential decay seen includes a superimposed nonsynaptic current. Tetraethylammonium injected into the presynaptic neurone produces only slight effect on the i.p.s.c. decay time constant, suggesting that the non‐synaptic current is unlikely to be due to a voltage‐dependent K conductance.This publication has 14 references indexed in Scilit:
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