Abstract
The rostral nucleus of the solitary tract (rNST), the initial CNS site for processing gustatory information, is comprised of two major cell types, glutamatergic excitatory and GABAergic inhibitory neurons. Although many investigators have described taste responses of rNST neurons, the phenotypes of these cells were unknown. To directly compare the response characteristics of both inhibitory and noninhibitory neurons, we recorded from mice expressing Channelrhodopsin-2 (ChR2) under the control of GAD65, a synthetic enzyme for GABA. We observed that chemosensitive profiles of GABAergic taste neurons (G+TASTE) were similar to non-GABA taste neurons (G-TASTE) but had much lower response rates. We further observed a novel subpopulation of GABA cells located more ventrally in the nucleus that were unresponsive to taste stimulation (G+UNR), suggesting pathways for inhibition initiated by centrifugal sources. This preparation also allowed us to determine how optogenetic activation of the rNST GABA network impacted the taste responses of G-TASTE neurons. Activating rNST inhibitory circuitry suppressed gustatory responses of G-TASTE neurons across all qualities and chemosensitive types of neurons. Although the tuning curves of identified G-TASTE were modestly sharpened, the overall shape of response profiles and the ensemble pattern remained highly stable. These neurophysiological effects were consistent with the behavioral consequences of activating GAD65-expressing inhibitory neurons using DREADDs. In a brief-access licking task, concentration-response curves to both palatable (sucrose, maltrin) and unpalatable (quinine) stimuli were shifted to the right when GABA neurons were activated. Thus, the rNST GABAergic network is poised to modulate taste intensity across the qualitative and hedonic spectrum.