Analysis of the Disruption in Hypothalamic-Pituitary Regulation in Rats Treated Neonatally with Monosodium L-Glutamate (MSG): Evidence for the Involvement of Tuberoinfundibular Cholinergic and Dopaminergic Systems in Neuroendocrine Regulation

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Abstract
Adult rats which received monosodium-L-glutamate (MSG) (4 mg/g body wt) on alternate days for the first 10 days of life acquired neurotoxic lesions of the retina and arcuate nucleus and manifested an endocrine deficiency syndrome characterized by stunted growth, obesity, hypothyroidism, hypogonadism and pituitary atrophy. The biochemical basis for the MSG-induced endocrine dysfunction was examined and the findings of note were as follows: normal serum levels of TSH [thyrotropin stimulating hormone] and LH [luteinizing hormone] despite hypothyroidism and gonadal atrophy, and significantly reduced serum GH [growth hormone] levels in both males and females; elevated serum PRL [prolactin] levels in males, but not females, normal or augmented pituitary release of LH and TSH to exogenous LHRH [LH releasing hormone] and TRH [thyrotropin releasing hormone]. Within the central nervous system: a normal diurnal rhythm of pineal N-acetyltransferase activity despite optic atrophy; normal concentrations of LHRH, TRH and somatostatin within the medial basal hypothalamus; normal concentrations of norepinephrine (NE), choline acetyltransferase (CAT) and dopamine (DA) in all extrahypothalamic regions examined; normal concentrations of serotonin (5HT) and NE, but greatly reduced concentrations of DA (40-50%) and CAT activity (70-75%) in the arcuate nucleus (ARC) and median eminence (ME) of the hypothalamus. From these findings several conclusions were drawn: The MSG-induced endocrine deficiency syndrome appears to result from the destruction of ARC-ME dopaminergic and cholinergic tuberoinfundibular systems within the hypothalamus; a normal concentration of serotonergic and noradrenergic neurons within the hypothalamus does not insure normal central neuroendocrine regulation; no more than 50% of the dopaminergic terminals in the ME arise from ARC perikarya; cell bodies within the ARC contribute very few, if any, nerve terminals containing releasing factors to the ME; MSG destroys the primary optic tracts while sparing the retino-hypothalamic projection; LHRH, somatostatin and TRH are not contained within cholinergic nerve terminals in the ME.