MONOSODIUM GLUTAMATE LESIONS INHIBIT THE N-METHYL-D-ASPARTATE-INDUCEDGROWTH-HORMONE BUT NOT PROLACTIN-RELEASE IN RATS

Large doses of glutamate administered to newborn rats damage permanent ly the neurones in the hypothalamic arcuate nucleus containing the gro wth hormone releasing hormone and the prolactin inhibiting dopamine ne uron cell bodies. Since adult animals that underwent neonatal glutamat e treatment still have a relatively well functioning growth hormone an d prolactin system, we tested whether in the adults the excitatory ami no acid sensibility is changed. After iv injection of different doses (10 or 30 mg/kg) of N-methyl-D-aspartate (excitatory amino acid recept or subtype agonist) growth hormone levels were significantly increased in the control groups but there was no rise in neonatally glutamate t reated male and female rats. The level of prolactin was increased by N -methyl-D-aspartate, too, but the glutamate treatment had no effect on the rise. Our study suggests that systemic administration of N-methyl -D-aspartate increases plasma growth hormone level by activating the g rowth hormone releasing cells in the arcuate nucleus, but the intact t uberoinfundibular dopaminergic pathway is not essential for its prolac tin stimulatory effect.