Evidence that reduced growth hormone secretion observed in monosodium glutamate-treated rats is the result of a deficiency in growth hormone-releasing factor.

The present experiments were designed to examine various aspects of GH secretion in adult male rats given monosodium glutamate (MSG; 4 mg/g BW, sc) during the neonatal period. MSG-treated animals sustained lesions localized to the hypothalamic arcuate nuclei (ARC) and had reduced nasal-anal lengths and body weights. Anterior pituitary (AP) weights were decreased, but AP concentrations of GH and PRL were not significantly altered. Analysis of pulsatile GH secretion showed depressed GH pulses and prolonged GH trough periods. Mean 5-h plasma GH levels were reduced, whereas PRL levels were not affected. Morphine sulfate (MS) at doses of 0.01, 0.1, 1.0, and 3.0 mg/kg induced a prompt rise in GH during the 45 min after drug administration in controls. MSG-treated animals showed a significant rise in GH only with 1.0 and 3.0 mg/kg MS. A significant elevation in PRL was found in both control and MSG-treated animals after 1.0 and 3.0 mg/kg MS. The pentobarbital-induced rise in GH was also blunted in MSG-treated animals. MSG-treated animals which were administered antisomatostatin serum showed elevated GH trough and mean GH levels, with no apparent effect on GH peak levels. In view of the mechanisms by which MS and pentobarbital act to increase GH secretion, the present data suggest that the GH regulatory deficit observed in MSG-treated rats is due to a relative loss of GH-releasing factor secondary to ARC damage.