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Our aims were to describe the mechanisms responsible for the sympathoinhibitory effects of SST on bulbospinal neurons and to identify likely sources of RVLM SST release. Patch clamp recordings were made from bulbospinal RVLM neurons (<jats:italic>n<\/jats:italic>\u2009=\u200931) in brainstem slices prepared from juvenile rat pups. Overall, 58% of neurons responded to SST, displaying an increase in conductance that reversed at \u221293 mV, indicative of an inwardly rectifying potassium channel (GIRK) mechanism. Blockade of sst<jats:sub>2<\/jats:sub>abolished this effect, but application of tetrodotoxin did not, indicating that the SST effect is independent of presynaptic activity. Fourteen bulbospinal RVLM neurons were recovered for immunohistochemistry; nine were SST\u2010insensitive and did not express sst<jats:sub>2a<\/jats:sub>. Three out of five responsive neurons were sst<jats:sub>2a<\/jats:sub>\u2010immunoreactive. Neurons that contained preprosomatostatin mRNA and cholera\u2010toxin\u2010B retrogradely transported from the RVLM were detected in: paratrigeminal nucleus, lateral parabrachial nucleus, K\u00f6lliker\u2010Fuse nucleus, ventrolateral periaqueductal gray area, central nucleus of the amygdala, sublenticular extended amygdala, interstitial nucleus of the posterior limb of the anterior commissure nucleus, and bed nucleus of the stria terminalis. Thus, those brain regions are putative sources of endogenous SST release that, when activated, may evoke sympathoinhibitory effects via interactions with subsets of sympathetic premotor neurons that express sst<jats:sub>2<\/jats:sub>. J. Comp. 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