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REVIEW: Nitric Oxide in Mechanisms of Brain Damage Induced by Neurotoxic Effect of Glutamate

V. G. Bashkatova* and K. S. Rayevsky

Institute of Pharmacology, Russian Academy of Medical Sciences, Baltiiskaya ul. 8, Moscow, 125315 Russia; fax: (095) 151-1261; E-mail: ksrayif@glasnet.ru

* To whom correspondence should be addressed.

Received February 26, 1998
Nitric oxide (NO) is a gaseous chemical messenger which plays the role of a universal modulator of various physiological functions of animals including the nervous system, i.e., interneuronal communications, synaptic plasticity, memory formation, receptor functions, intracellular signal transmission, release of neurotransmitters. The possible role of NO is considered in some basic diseases of the central nervous system which are associated with the neurotoxic effect of glutamate (ischemia, stroke, convulsive disorders, etc.). NO is believed to be a key pathophysiological factor of these diseases. The production of NO in the brain cortex of rats was found to significantly increase during convulsions of various origin.
KEY WORDS: nitric oxide, NO-synthase, glutamate receptors, brain ischemia, convulsions, lipid peroxidation, EPR spectroscopy