Perturbation of amygdala/somatostatin-nucleus of the solitary tract projections reduces sensitivity to quinine in a brief-access test.

Neural processing in the nucleus of the solitary tract (NST) is critical for concentration-dependent intake of normally preferred and avoided taste stimuli (e.g. affective responding); and is influenced by descending input from numerous forebrain regions. In one region, the central nucleus of the amygdala (CeA), a subpopulation of neurons that project to the NST express the neuropeptide somatostatin (Sst). The present study investigated whether this CeA/Sst-to-NST pathway contributes to concentration-dependent intake of sucrose and quinine hydrochloride (QHCl) solutions using brief-access lick trials (5 s). In both female and male mice, we used virus-based optogenetic tools and laser light illumination to manipulate the activity of CeA/Sst neurons that project to the NST. During light-induced inhibition of CeA/Sst-to-NST neurons, mice licked significantly more to our three highest concentrations of QHCl compared to control mice, while sucrose intake was unaffected. Interestingly, light-induced activation of this descending pathway did not influence licking of either sucrose or QHCl. These findings suggest that the CeA/Sst-to-NST pathway must be active for normal affective responding to an exemplary aversive taste stimulus.