REVIEW: Cellular Mechanisms of Brain Hypoglycemia

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N. K. Isaev^1,2*, E. V. Stel'mashuk², and D. B. Zorov¹

¹Belozersky Institute of Physico-Nhemical Biology, Lomonosov Moscow State University, 119992 Moscow, Russia; fax: (495) 939-3181; E-mail: isaev@genebee.msu.su

²Institute of Neurology, Russian Academy of Medical Sciences, Pereulok Obukha 5, 105064 Moscow, Russia

^* To whom correspondence should be addressed.

Received October 24, 2006; Revision received January 15, 2007

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Data on intracellular processes induced by a low glucose level in nerve tissue are presented. The involvement of glutamate and adenosine receptors, mitochondria, reactive oxygen species (ROS), and calcium ions in the development of hypoglycemia-induced damage of neurons is considered. Hypoglycemia-induced calcium overload of neuronal mitochondria is suggested to be responsible for the increased ROS production by mitochondria.

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KEY WORDS: hypoglycemia, glucose, neurons, mitochondria, free radicals, calcium

DOI: 10.1134/S0006297907050021

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