Enhancing effects of beta-endorphin on glutamate neurotoxicity.

AIM: To study the effect of beta-endorphin (beta-End) on monosodium glutamate (MSG)-induced neurotoxicity (GNT). METHODS: Image analysis of neuronal areas and determination of mitochondrial membrane protein-bound Ca2+ and intracellular free Ca2+ ([Ca2+]i) were used. RESULTS: beta-End aggravated MSG-induced neuronal injury in arcuate nucleus of hypothalamus in a dose-dependent manner in the range from 0.5 to 5.0 mg.kg-1. MSG-induced increase in mitochondrial membrane protein-bound Ca2+ was enhanced when treated with beta-End 2 g.L-1. MSG-induced elevation in [Ca2+]i in single neuron was also augmented from 320 +/- 84 to 589 +/- 78 nmol.L-1 by the treatment with beta-End 2 g.L-1. CONCLUSION: beta-End enhanced GNT via aggravating the disruption of intracellular Ca2+ homeostasis induced by MSG.