Selective alterations of opiate receptor subtypes in monosodium glutamate-treated rats.

Abstract

Neonatal treatment of rats with monosodium glutamate (MSG) has been demonstrated to destroy cell bodies of neurons in the arcuate nucleus including the brain beta-endorphin (B-END) system. The effects on opiate receptors of the loss of B-END is unknown. Neonatal rats were treated with MSG as previously described. After reaching maturity (7-9 months), MSG-treated rats and litter-matched untreated control rats were decapitated and brains dissected into brain regions. Opiate receptor assays were run with [3H]morphine (mu receptor ligand) and [3H]D-alanine2-D-leucine5 (DADL) enkephalin (delta receptor ligand) for each brain region for both MSG and control rats simultaneously. Scatchard plot analyses showed a selective increase in delta receptors in the thalamus only. No corresponding change in mu receptors in the thalamus was found. The cross-competition IC50 data supported this conclusion, showing a loss in the potency of morphine in displacing [3H]DADL enkephalin in the thalamus of MSG-treated rats. This shift in delta receptors produced an IC50 displacement pattern in thalamus, ordinarily a mu-rich area, similar to that of striatum or cortex, delta-rich areas, again indicating an increase in delta receptors. Similar changes in delta receptors in other brain regions were not found. These results represent one of the few examples of a selective and localized shift in delta with no change in mu sites. Furthermore, the delta increase may reflect an up-regulation of the receptors in thalamus after chronic loss of the endogenous opioid B-END.