Release of endogenous amino acid neurotransmitter candidates from rat olfactory cortex slices: Possible regulatory mechanisms and the effects of pentobarbitone

Abstract

A study has been made of the regulation of evoked release of the amino acid neurotransmitter candidates (aspartate, GABA and taurine) from rat olfactory cortex slices. The effects of pentobarbitone (10–1000 μM) on release have also been assessed. Release of aspartate, the presumed excitatory transmitter of some of the lateral olfactory tract fibres, is reduced by muscimol (10 μM) and this effect is antagonized by picrotoxin (15 μM): it is concluded that presynaptic GABA receptors may modulate aspartate release. Low concentrations of pentobarbitone also reduce aspartate release, but this effect is picrotoxin-insensitive. Release of GABA, the presumed transmitter of inhibitory interneurones, is reduced by muscimol (10 μM) and this effect is antagonized by picrotoxin (15 μM): it is suggested that GABA release may be regulated by presynaptic autoreceptors. Pentobarbitone significantly increases release of GABA when slices are synaptically activated although the mechanism of this effect is nuclear. Release of taurine, not hitherto considered a neurotransmitter in this brain area, is depressed by muscimol (10 μM) and pentobarbitone and increased by picrotoxin (15 μM). Results are discussed in terms of (i) mechanisms of regulation of amino acid release in the olfactory cortex, (ii) effects of pentobarbitone on release and(iii) the compatibility of the present results with previously published electrophysiological studies.