Monosodium glutamate lesions inhibit the N-methyl-D-aspartate-induced growth hormone but not prolactin release in rats.

Large doses of glutamate administered to newborn rats damage permanently the neurones in the hypothalamic arcuate nucleus containing the growth hormone releasing hormone and the prolactin inhibiting dopamine neuron cell bodies. Since adult animals that underwent neonatal glutamate treatment still have a relatively well functioning growth hormone and prolactin system, we tested whether in the adults the excitatory amino acid sensibility is changed. After i.v. injection of different doses (10 or 30 mg/kg) of N-methyl-D-aspartate (excitatory amino acid receptor subtype agonist) growth hormone levels were significantly increased in the control groups but there was no rise in neonatally glutamate treated 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 growth hormone releasing cells in the arcuate nucleus, but the intact tuberoinfundibular dopaminergic pathway is not essential for its prolactin stimulatory effect.