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Enhancing effects of Herpesvirus hominis on sodium glutamate neurotoxicity

  
@article{APS6194,
	author = {Juan Wu and Jing Gao and Xiao-ning Zhao and Ying Wu and Zu-xuan Zhang},
	title = {Enhancing effects of Herpesvirus hominis on sodium glutamate neurotoxicity},
	journal = {Acta Pharmacologica Sinica},
	volume = {15},
	number = {2},
	year = {2016},
	keywords = {},
	abstract = {The neurotoxic effects of sodium glutamate (MSG, 2.5 g.kg-1 sc) and the enhancing effects of neurotropic Herpesvirus hominis (HVH, 0.2 ml/mouse ip) on MSG toxicity were studied through histomorphological observations, together with detection of the concentration of both mitochondrial protein bound Ca2+ and intracellular free Ca2+ ([Ca2+]i) by the Tb3+ fluorescent probe and Ca2+ indicator Fura-2/AM, respectively. It was found that in 10-d-old mice the neurons in arcuate hypothalamic nucleus degenerated severely after treatment with HVH+MSG, showing swollen edematous cytoplasm, dark pyknotic nuclei as well as a decrease in the amount of the neurons. The hypothalamic and spinal cord mitochondrial Tb3+ relative fluorescent intensity increased from 20 +/- 3 and 20 +/- 1 to 28 +/- 5 and 34 +/- 6, ie, the mitochondrial protein bound Ca2+ reduced significantly. MSG elevated the [Ca2+]i levels from 0.11 +/- 0.03 to 0.69 +/- 0.19 mumol.L-1 by not only stimulating the Ca2+ influx but also releasing the Ca2+ from intracellular stores. These findings suggested that MSG neurotoxicity was probably related to the overloading of neuroplasmic Ca2+, the destruction of neuronal abilities to deplete or sequester the intracellular Ca2+, as well as the irreversible neuronal injury and death.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/6194}
}