Neurochemical phenotype of sympathetic nervous system outflow from brain to white fat

Citation
Hf. Shi et Tj. Bartness, Neurochemical phenotype of sympathetic nervous system outflow from brain to white fat, BRAIN RES B, 54(4), 2001, pp. 375-385
Citations number
28
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH BULLETIN
ISSN journal
03619230 → ACNP
Volume
54
Issue
4
Year of publication
2001
Pages
375 - 385
Database
ISI
SICI code
0361-9230(20010301)54:4<375:NPOSNS>2.0.ZU;2-Y
Abstract
The sympathetic innervation of white adipose tissue (WAT) appears to be a d ominant mechanism triggering lipolysis. The purpose of this study was to de termine the neurochemical phenotype of neurons comprising the sympathetic o utflow from brain to WAT. This was accomplished by injecting Siberian hamst er WAT with a viral retrograde transneuronal tract tracer, the pseudorabies virus (PRV), in combination with immunocytochemical characterization of se veral neurotransmitters or their synthetic enzymes in the brain. Catecholam inergic (tyrosine hydroxylase [TH] and dopamine-beta -hydroxylase [DBH] imm unoreactivity) and peptidergic (arginine vasopressin [AVP] and oxytocin [OX Y] immunoreactivity) neurons were part of this outflow, but the percentage of double-labeled cells was small, consistent with previous studies. Brains tem PRV + TH-or PRV + DBH-labeled cells were in previously identified norad renergic areas (A5, A6, and subcoeruleus, rostroventrolateral medulla [RVL] , some reticular nuclei). Forebrain double labeling was greatest in the par aventricular (TH, AVP, OXY) and suprachiasmatic (AVP) nuclei, both implicat ed in the central control of lipolysis. Differences between the PRV double labeling reported here for WAT versus that of other sympathetic peripheral targets were PRV + DBH in A5 and RVL, and PRV + TH in RVL and in the latera l paragigantocellular and lateral reticular nuclei. Collectively, these res ults begin to identify the neurochemical identity of the sympathetic outflo w from brain to WAT. (C) 2001 Elsevier Science Inc.