Neonatal Monosodium Glutamate Treatment Alters the Response of Median Eminence Luteinizing Hormone-Releasing Hormone Nerve Terminals to Potassium and Prostaglandin E2*

Publisher Website
Google Scholar
Abstract
The following study was designed to examine the effect of neonatal monosodium glutamate (MSG) treatment on: 1) the distribution of LHRH in discrete regions of the hypothalamus and 2) the response of median eminence (ME) LHRH terminals to two secretogogues using an in vitro superfusion system. Adult male rats (5 months old) treated with MSG during the first 10 days of life displayed the characteristic endocrine abnormalities previously associated with this syndrome. In addition, ME fragments from MSG-treated rats weighed significantly less (P < 0.01) and had a significantly lower (P < 0.05) protein content than similar fragments obtained from control male rats, suggesting that the ME is atrophic after MSG treatment. Concentrations of LHRH (picograms per μg protein) were significantly decreased (P < 0.05) in the arcuate nucleus and increased (P < 0.01) in the ME of MSG-treated rats compared with LHRH levels measured in control rats. Whereas dopamine levels were significantly reduced (P < 0.01) in the arcuate nucleus of MSG-treated rats, levels of this amine measured in the ME or posterior lobe did not differ from control values. Basal LHRH release (picograms per mg/min) by superfused ME fragments (two MEs per chamber) from MSG-treated rats initially was higher than release by control MEs, whereas at 50 min, LHRH release rates were similar in both groups. Superfusion with a high potassium (30 HIM) medium elicited greater and faster increases in LHRH secretion by ME fragments from MSG-treated rats than by control ME fragments. Injection of prostaglandin E2 resulted in rapid increases in LHRH release by ME fragments from both groups of rats; however, release of this decapeptide by ME fragments from MSG-treated rats was 2-to 3-fold higher than release by control fragments. These results show that ME LHRH terminals in MSG-treated rats are hyperresponsive to both high K+ and prostaglandin E2 stimulation and indicate that the mechanism (s) that normally triggers LHRH release is defective in these animals. The hyper-responsiveness of the ME LHRH terminals may result from denervation of the LHRH neurons due, at least in part, to the loss of dopamine neurons in the arcuate.

This publication has 15 references indexed in Scilit: