Enhancing effects of beta-endorphin on glutamate neurotoxicity.
OBJECTIVE
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.


CONCLUSIONS
beta-End enhanced GNT via aggravating the disruption of intracellular Ca2+ homeostasis induced by MSG.
Zhu
L
L
School of Medicine, Nanjing University, China.
Gao
J
J
Wu
J
J
Zhao
X N
XN
Zhang
Z X
ZX
D000818:Animals; D000831:Animals, Newborn; D001111:Arcuate Nucleus of Hypothalamus / Q000473:pathology*; D001921:Brain / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D005260:Female; D007091:Image Processing, Computer-Assisted; D008297:Male; D051379:Mice; D008928:Mitochondria / Q000378:metabolism; D012970:Sodium Glutamate; D001615:beta-Endorphin / Q000494:pharmacology*
D001615:beta-Endorphin; D002118:Calcium; D012970:Sodium Glutamate