There is increasing evidence, both electrophysiological and behavioral, that bitter and sweet stimuli drive parallel pathways in the gustatory brainstem. Here we report two lines of investigation that suggest significant interactions among these parallel systems. First, responses recorded from single cells in the hamster's parabrachial nuclei (PbN) show that quinine hydrochloride (QHCl) produces a substantial suppression (> 40%) of the responses of PbN cells to sucrose. Sucrose stimulation has a reciprocal suppressive effect on the response to QHCl. These results imply that aversive and appetitive stimuli produce mutual inhibition in the gustatory system; studies of the chorda tympani nerve response suggest that this inhibition likely arises within the brainstem. A second line of investigation, using both an in vitro brainstem slice preparation and in vivo pharmacological manipulations of cells in the hamster NST, has demonstrated an inhibitory network within the rostral NST that plays a role in the modulation of taste activity. Patch-clamp and extracellular recording studies in vitro show that cells within the rostral central subdivision of the NST are inhibited by gamma-aminobutyric acid (GABA); this mediation is largely through the GABAA receptor subtype. Here we show that responses to taste stimulation recorded extracellularly from NST cells in vivo can be inhibited by local microinjections of GABA; this inhibition is blocked by the GABAA receptor antagonist bicuculline methiodide. Responses to sucrose are significantly more inhibited than those to NaCl or KCl. These combined lines of evidence show that appetitive and aversive stimuli activate mutually inhibitory systems within the brainstem and suggest that the basis for this interaction is a GABAergic inhibitory network within the NST.(ABSTRACT TRUNCATED AT 250 WORDS)