Interactions between neurons and astrocytes in the turnover of GABA and glutamate

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Abstract

Interactions between neurons and astrocytes in the turnover of GABA and its precursor glutamate (which probably is a transmitter in its own right) are reviewed on the basis of observations in preparations of specific cell types. It is concluded that GABA is released predominantly from neurons. Subsequently, the released GABA molecules may (a) be reaccumulated by nerve endings, (b) be accumulated and metabolized by nonsynaptosomal parts of the neurons, or (c) be accumulated and metabolized by astrocytes. Each of these processes seems to occur to a physiologically important extent but the factor(s) deciding which of these three events will take place are unknown. Glutamate is released in larger amounts than GABA and accumulated almost exclusively into astrocytes. Functionally important differences probably exist between uptake mechanisms into neurons and into astrocytes, e.g., in the quantitative correlation between transport of GABA (or glutamate) and sodium transport. It is not known to what extent glutamine is returned from astrocytes to neurons to compensate for the release of GABA and glutamate.

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