MSG effects on beta-endorphin and alpha-MSH in the hypothalamus and caudal medulla

Abstract

Monosodium glutamate (MSG) was given to neonatal male rats to determine its effects on neurons containing beta-endorphin ([beta]-END) and alpha-melanocyte stimulating hormone ([alpha]-MSH) within the basal hypothalamus (arcuate nucleus) and caudal medulla [nucleus tractus solitarius (NTS)] and on the levels of [beta]-END and [alpha]-MSH within these areas. Immunocytochemical studies demonstrated a reduction in the number of cells within the medial hypothalamic area (arcuate nucleus) amon MSG-treated animals versus saline controls. MSG did not reduce the number of cell bodies within the caudal medulla (NTS). MSG significantly reduced [beta]-END and [alpha]-MSH immunoreactive levels in the basal hypothalamus as determined by radioimmunoassay. Whereas a significant reduction in the level of [beta]-END occurred in the ventral caudal medulla (VCM), none occurred in the dorsal caudal medulla (DCM). In contrast, levels of [alpha]-MSH increased significantly in the DCM among animals receiving MSG compared to control animals. This study documents the contribution of beta-endorphin containing neurons of the basal hypothalamus to areas of the caudal medulla. The effect of MSG on beta-endorphin and [alpha]-MSH neurons in these areas and their differential effects on levels in the caudal medulla areas raises questions about the sites of origin of these peptides.