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Somatostatin in the rat rostral ventrolateral medulla: Origins and mechanism of action
Author(s) -
Bou Farah Lama,
Bowman Belinda R.,
Bokiniec Phil,
Karim Shafinaz,
Le Sheng,
Goodchild Ann K.,
McMullan Simon
Publication year - 2015
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.23846
Subject(s) - rostral ventrolateral medulla , neuroscience , lateral parabrachial nucleus , brainstem , central nucleus of the amygdala , chemistry , medulla oblongata , nucleus , stria terminalis , amygdala , area postrema , biology , central nervous system , parabrachial nucleus
Somatostatin (SST) or agonists of the SST‐2 receptor (sst 2 ) in the rostral ventrolateral medulla (RVLM) lower sympathetic nerve activity, arterial pressure, and heart rate, or when administered within the Bötzinger region, evoke apneusis. 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 ( n = 31) in brainstem slices prepared from juvenile rat pups. Overall, 58% of neurons responded to SST, displaying an increase in conductance that reversed at −93 mV, indicative of an inwardly rectifying potassium channel (GIRK) mechanism. Blockade of sst 2 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‐insensitive and did not express sst 2a . Three out of five responsive neurons were sst 2a ‐immunoreactive. Neurons that contained preprosomatostatin mRNA and cholera‐toxin‐B retrogradely transported from the RVLM were detected in: paratrigeminal nucleus, lateral parabrachial nucleus, Kölliker‐Fuse 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 2 . J. Comp. Neurol. 524:323–342, 2016. © 2015 Wiley Periodicals, Inc.