Developmental and sex-specific effects of low dose neonatal monosodium glutamate administration on mediobasal hypothalamic chemistry.

Abstract

Neonatal administration of monosodium glutamate (MSG) to rodents results in severe damage to the arcuate nucleus of the hypothalamus (AN). MSG-induced AN damage produces profound alterations in hypothalamic neurotransmitters and anterior pituitary function. Reproductive function is also severely compromised in both male and female MSG-treated rats. The present study investigated the developmental sequelae of MSG-induced alterations in hypothalamic monoamine metabolism as well as other aspects of MSG toxicity. Female rats given 4 mg/g of MSG on postnatal days 2 and 4 did not exhibit any significant alterations in hypothalamic monoamine metabolism on postnatal days 21 or 30, however, postpubertal MSG-treated females had significantly reduced levels of mediobasal hypothalamic (MBH) dopamine and DOPAC. In contrast, male MSG-treated rats had slight reductions in hypothalamic and MBH dopamine levels but these reductions were not statistically significant. Male MSG-treated rats did exhibit significant reductions in hypothalamic DOPAC on postnatal day 30 and MBH homovanillic acid (HVA) levels on day 100. Acetylcholine levels were also measured in the MBH and pituitary of adult male MSG-treated rats and found to be unaltered. The developmental profile of hypothalamic monoamines and their metabolites and MSG-induced alterations in dopamine and DOPAC levels in the MBH of female rats are discussed in relation to the neurochemical mechanisms involved in triggering puberty.