[Effects of beta-endorphin on glutamate neurotoxicity].
The effects of beta-endorphin(beta-End) on monosodium glutamate(MSG) neurotoxicity were studied via morphological observation and image analysis of neuronal areas, together with the determination of intracellular free calcium concentration ([Ca2+]i) in single neuron and radioimmunoassay for beta-End contents. beta-End(1.0 mg.kg-1, s.c.) was found to obviously aggravate the neuronal injury in the arcuate nucleus of hypothalamus induced by MSG(0.5 g.kg-1, s.c.). Just as MSG increased [Ca2+]i significantly, beta-End(2.0 g.L-1) itself also increased it, though the extent of elevation was smaller than that of MSG(17.0 mg.L-1). The obvious changes of [Ca2+]i induced by both MSG and beta-End were partially reversed after pretreatment with verapamil. On the other hand, the content of beta-End in different areas of the brain were augmented following the addition of MSG and further elevated by morphine treatment. These findings suggest that the mechanisms of the enhancing effect of beta-End on glutamate neurotoxicity were linked to the aggravation on the disruption of intracellular Ca2+ homeostasis induced by MSG. Moreover, the fact that opioids promote beta-End release induced by MSG may be involved in the mechanisms as well.
Gao
J
J
Department of Pharmacology, School of Medicine, Nanjing University, Nanjing 210093.
Zhu
L
L
Zhao
X
X
Zhang
Z
Z
D000818:Animals; D000831:Animals, Newborn; D001111:Arcuate Nucleus of Hypothalamus / Q000473:pathology; D001921:Brain / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D005260:Female; D007031:Hypothalamus / Q000473:pathology; D008297:Male; D051379:Mice; D009474:Neurons / Q000378:metabolism; D020258:Neurotoxicity Syndromes / Q000209:etiology / Q000473:pathology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012970:Sodium Glutamate; D001615:beta-Endorphin / Q000494:pharmacology*
D001615:beta-Endorphin; D002118:Calcium; D012970:Sodium Glutamate