Corticotropin-releasing hormone synthesizing neurons in the hypothalamic paraventricular nucleus of rats neonatally treated with monosodium glutamate can respond to different stress paradigms.

Neonatal administration of monosodium glutamate (MSG) produces pathological lesions in many brain regions. There are indications that MSG treatment could also influence the neurons of the hypothalamic paraventricular nucleus (PVN). The goal of this study was to find out whether MSG treatment could alter the activity of the corticotropin-releasing hormone synthesizing neurons, i.e. the principal regulators of the corticotropin hormone secretion, located in the medial posterior subdivision of the PVN. The activity of CRH neurons was assessed by changes in CRH mRNA levels in response to both stimulatory and inhibitory conditions induced by immobilization and water deprivation, respectively. In addition, effect of the circulating glucocorticoid deficit induced by bilateral adrenalectomy was investigated. The obtained data show that in MSG-treated animals the rise in CRH mRNA in response to immobilization stress and adrenalectomy as well as the decrease after water deprivation were similar to the changes seen in controls. In addition POMC mRNA changes in MSG-treated animals indicate an uninterrupted capability of CRH neurons to transform different signals to corticotropin cells. It can be concluded that CRH neurons of the PVN are not functionally altered, in spite of the widespread neurotoxic effect of MSG treatment.