Influence of GABA on neurons of the gustatory zone of the rat nucleus of the solitary tract

Abstract

The role of [gamma]-aminobutyric acid (GABA) as an inhibitory neurotransmitter in the rostral, gustatory zone of the nucleus of the solitary tract (rNST) was examined using whole cell recordings in brain slices of the adult rat medulla. Superfusion of GABA resulted in a concentration-dependent reduction in input resistance in 68% of the neurons in rNST. The change in input resistance was often accompanied by membrane hyperpolarization. The effect of GABA was a direct action on the postsynaptic membrane since it could be elicited when synaptic transmission was blocked by tetrodotoxin or in a low Ca2+ and high Mg2+ perfusing solution. The mean reversal potential of the GABA effect was about -60 mV, determined by applying GABA at different holding potentials, or from the intersection of current-voltage curves measured in control saline and saline containing GABA. When neurons were separated into groups based on intrinsic membrane properties, some neurons in each group responded to GABA. Superfusion of the slices with either the GABAA agonist, muscimol, or the GABAB agonist, baclofen, caused a decrease in input resistance accompanied by membrane hyperpolarization. The GABAA antagonist bicuculline either totally or partially blocked the neuronal response to GABA and blocked the response to muscimol but did not antagonize responses to baclofen. Superfision of the GABAB antagonist phaclofen depressed the membrane responses to GABA. The use of the GABAA and GABAB agonists and antagonists demonstrates that some neurons in rNSt have both GABAA and GABAB receptors. Since most rNST neurons studied respond to GABA, inhibition probably plays a major role in sensory processing by the rNST.