REVIEW: Role of Mitochondria in the Mechanisms of Glutamate Toxicity

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N. K. Isaev^1*, N. A. Andreeva², E. V. Stel'mashuk², and D. B. Zorov¹

¹Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119992 Moscow, Russia; fax: (7-095) 939-3181; E-mail: isaev@genebee.msu.su

²State Brain Research Institute, Russian Academy of Medical Sciences, 105064 Moscow, Russia

^* To whom correspondence should be addressed.

Received March 23, 2004; Revision received July 6, 2004

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Current data on glutamate-induced functional and morphological changes in mitochondria correlating with or being a result of their membrane potential changes are reviewed. The important role of Ca²⁺, Na⁺, and H⁺ in the potentiation of such changes is considered. It is assumed that glutamate-induced loss of mitochondrial potential is mediated by Ca²⁺ overload resulting in the induction of nonspecific permeability of the inner mitochondrial membrane.

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KEY WORDS: neurons, mitochondria, glutamate, calcium ions

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