Voltage dependence of Ia reciprocal inhibitory currents in cat spinal motoneurones.
AUTOR(ES)
Stuart, G J
RESUMO
1. Inhibitory postsynaptic currents (IPSCs) were recorded in voltage clamped posterior biceps or semitendinosus motoneurones of the cat during reciprocal inhibition. 2. Population IPSCs, recorded following stimulation of the whole quadriceps muscle nerve, had an average time-to-peak of 0.51 +/- 0.02 ms (+/- S.E.M., n = 22) and decayed exponentially, with an average time constant of 0.99 +/- 0.04 ms (at 37 degrees C) at resting membrane potentials. 3. Unitary IPSCs, recorded following spike-triggered averaging from an identified reciprocal inhibitory interneurone, had amplitudes of 120-220 pA with an average time-to-peak of 0.40 +/- 0.06 ms (n = 5). The decay of these unitary currents was exponential, with an average time constant of 0.82 +/- 0.07 ms (at 37 degrees C) at resting membrane potentials. 4. The time course of IPSCs was unaffected by either alpha-chloralose or pentobarbitone at concentrations necessary for deep anaesthesia. 5. The peak synaptic current varied linearly with the membrane potential over the range -90 to -30 mV, and had an average reversal potential of -80.7 +/- 1.5 mV (+/- S.E.M., n = 6) when measured using KCH3SO4-filled electrodes. 6. The reversal potential for the IPSC was used to calculate [Cl-]i. This was estimated to be 6.5 mM assuming that the inhibitory synaptic current was mediated purely by Cl- ions. 7. The rate at which synaptic currents decayed was exponentially dependent on the postsynaptic membrane potential, the decay time constant increasing e-fold for a 91 mV depolarization. This result was independent of [Cl-]i or of the magnitude of the synaptic conductance and was interpreted as a voltage dependence of the glycine channel open time. 8. The average unitary peak conductance was 9.1 +/- 1.7 nS (+/- S.E.M., n = 5), corresponding to the opening of approximately 200 glycine-activated postsynaptic channels following neurotransmitter release from a single Ia reciprocal interneurone.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1190040Documentos Relacionados
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