Rostral forebrain structures, such as the central nucleus of the amygdala (CeA), send projections to the nucleus of the solitary tract (NST) and the parabrachial nucleus (PBN) that modulate taste-elicited responses. However, the proportion of forebrain-induced excitatory and inhibitory effects often differs when taste cell recording changes from the NST to the PBN. The present study investigated whether this descending influence might originate from a shared or distinct population of neurons marked by expression of somatostatin (Sst). In Sst-reporter mice, the retrograde tracers’ cholera toxin subunit B AlexaFluor-488 and -647 conjugates were injected into the taste-responsive regions of the NST and the ipsilateral PBN. In Sst-cre mice, the cre-dependent retrograde tracers’ enhanced yellow fluorescent protein Herpes Simplex Virus (HSV) and mCherry fluorescent protein HSV were injected into the NST and the ipsilateral PBN. The results showed that ~40% of CeA-to-PBN neurons expressed Sst compared with ~ 23% of CeA-to-NST neurons. For both the CeA Sst-positive and -negative populations, the vast majority projected to the NST or PBN but not both nuclei. Thus, a subset of CeA-to-NST and CeA-to-PBN neurons are marked by Sst expression and are largely distinct from one another. Separate populations of CeA/Sst neurons projecting to the NST and PBN suggest that differential modulation of taste processing might, in part, rely on differences in local brainstem/forebrain synaptic connections.

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