Pentobarbitone interference with inhibitory synaptic transmission in crayfish stretch receptor neurones.

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Abstract
The effect of pentobarbitone (PB) on GABA-ergic inhibition was investigated in the isolated crayfish stretch receptor. The soma of the slowly adapting neuron was impaled with 2 micro-electrodes to give an accurate determination of membrane conductances. Application of PB in concentrations from 10-6-10-3 M increased the rise time constant of the inhibitory post-synaptic potential (IPSP). The IPSP percentage amplitude and decay time constant were also increased in 8 of 12 neurons. On prolonged exposure, percentage amplitude declined at a rate dependent upon the dose and the frequency of stimulation until the IPSP became undetectable. The response to ionophoretically applied GABA remained essentially unaltered in the presence of PB, but the falling phase was prolonged by up to 8% in 4 of the 10 neurons tested. Resting membrane conductance, IPSP driving force (IPSP reversal potential minus resting membrane potential) and parameters of the anti and orthodromic action potential were not significantly affected. Removal of PB after prolonged exposure usually caused an immediate increase in IPSP percentage amplitude, but the IPSP rising phase remained slowed. Application of excess extracellular GABA only affected the IPSP percentage amplitude after it had been reduced by PB. It transiently increased the attenuated IPSP percentage amplitude in the presence of PB, and after the removal of PB permanently increased the amplitude to its original value. Nipecotic acid and cis-1,3-aminocyclohexane carboxylic acid, inhibitors of GABA re-uptake, slightly increased the IPSP percentage amplitude, and prolonged the falling phase but did not affect the rising phase. Percentage amplitude declined on prolonged exposure. PB has no electrophysiologically demonstrable post-synaptic action in the crayfish stretch receptor neuron, but it inhibits the presynaptic release and re-uptake of GABA.