Somatostatin neurons in the rostral nucleus of the solitary tract are functionally heterogeneous.

The rostral nucleus of the solitary tract (rNST) is the initial central site for taste processing. This nucleus has a complex circuitry and multiple cell types with different response properties, connectivity, and morphology (Travers and Travers 2018). However, unlike its visceral counterpart, the caudal NST, neurochemical phenotypes in rNST are poorly defined. Recent studies have begun to probe this gap. Based on fiber photometry, optogenetics, and cell-type specific deletion. For example, one group proposed that somatostatin (SST) rNST neurons, neither calbindin or dynorphin cells, responded specifically to bitter stimuli and that these neurons were necessary for suppression of quinine-induced licking (Jin, Fishman et al. 2021) (Zhang, Jin et al. 2019). The present study employed in situ hybridization, optotagging, and chemogenetic suppression in male and female mice to demonstrate that SST neuron function is more complex. Although most SST neurons responded optimally to bitter stimuli, many others were activated by different qualities and some non-SST neurons responded to bitter tastants. Moreover, roughly equal proportions of SST neurons expressed excitatory (VGLUT2) or inhibitory (VGAT) markers. Suppressing SST neural activity with DREADDS enhanced licking to both quinine and sucrose suggesting that neural activity elicited by the aversive bitter stimulus was suppressed whereas licking elicited by the sweet, preferred stimulus was increased. We hypothesize that these effects arise from suppressing excitatory quinine-responsive SST neurons but that a separate population of inhibitory SST neurons synapse on sucrose-responsive cells.