AIM: To study the effects of beta-endorphin (beta-End) on monosodium g
lutamate (MSG)-induced neurotoxicity (GNT). METHODS: Image analysis of
neuronal areas and determination of mitochondrial membrane protein-bo
und Ca2+ and intracellular free Ca2+ ([Ca2+](i)) were used, RESULTS: b
eta-End aggravated MSG-induced neuronal injury in arcuate nucleus of h
ypothalamus in a dose-dependent manner in the range from 0.5 to 5.0 mg
. kg(-1). MSG-induced increase in mitochondrial membrane protein-boun
d 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.