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

Abstract

Many animals show seasonal changes in adiposity that are triggered by changes in the photoperiod. For example, in short “winterlike” days, the nocturnal duration of pineal melatonin (MEL) secretion increases ultimately resulting in body fat decreases by Siberian hamsters. These decreases in body fat are mediated through increases in the sympathetic drive on white adipose tissue (WAT). The central nervous system (CNS) origins of the sympathetic outflow from brain to WAT include the suprachiasmatic nucleus (SCN), an area necessary for the reception of season-encoded MEL signals in Siberian hamsters. Therefore, we tested whether SCN neurons that are part of the sympathetic outflow to WAT also express MEL receptors (MEL1a). This was accomplished by labeling the sympathetic outflow from brain to WAT using a transsynaptic retrograde tract tracer, the pseudorabies virus (PRV), injected into inguinal WAT combined with labeling of brain MEL1areceptors using in situ hybridization. We found PRV-labeled neurons that also expressed MEL1a-receptor mRNA in several brain regions including the SCN. Thus the increased duration of MEL secretion in short days may increase MEL1a-receptor stimulation that, in turn, increases the sympathetic drive on WAT, thereby increasing lipolysis and decreasing adiposity.