CNS sympathetic outflow neurons to white fat that express MEL receptors may mediate seasonal adiposity

Citation
Ck. Song et Tj. Bartness, CNS sympathetic outflow neurons to white fat that express MEL receptors may mediate seasonal adiposity, AM J P-REG, 281(2), 2001, pp. R666-R672
Citations number
48
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
281
Issue
2
Year of publication
2001
Pages
R666 - R672
Database
ISI
SICI code
0363-6119(200108)281:2<R666:CSONTW>2.0.ZU;2-A
Abstract
Many animals show seasonal changes in adiposity that are triggered by chang es in the photoperiod. For example, in short "winterlike" days, the nocturn al duration of pineal melatonin (MEL) secretion increases ultimately result ing in body fat decreases by Siberian hamsters. These decreases in body fat are mediated through increases in the sympathetic drive on white adipose t issue (WAT). The central nervous system (CNS) origins of the sympathetic ou tflow from brain to WAT include the suprachiasmatic nucleus (SCN), an area necessary for the reception of season-encoded MEL signals in Siberian hamst ers. Therefore, we tested whether SCN neurons that are part of the sympathe tic outflow to WAT also express MEL receptors (MEL1a). This was accomplishe d by labeling the sympathetic outflow from brain to WAT using a transsynapt ic retrograde tract tracer, the pseudorabies virus (PRV), injected into ing uinal WAT combined with labeling of brain MEL1a receptors using in situ hyb ridization. We found PRV-labeled neurons that also expressed MEL1a-receptor mRNA in several brain regions including the SCN. Thus the increased durati on of MEL secretion in short days may increase MEL1a-receptor stimulation t hat, in turn, increases the sympathetic drive on WAT, thereby increasing li polysis and decreasing adiposity.