Journal
NEUROCHEMICAL RESEARCH
Volume 26, Issue 6, Pages 661-666Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1023/A:1010939304104
Keywords
astrocytes; glutamatergic neurons; glutamate-transporters; glutamate; depolarization; heteroexchange; uptake; release
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Uptake and release processes in cerebellar astrocytes and granule neurons (glutamatergic) for glutamate were investigated by the use of [H-3]D-aspartate. a non-metabolizable glutamate analog. The effects of DL-threo-beta -benzyloxyaspartate (DL-TBOA) and L-trans-pyrrolidine-2,4-dicarboxylate (t-2,4-PDC) on uptake and release of [H-3]D-aspartate were studied. Both compounds inhibited potently uptake of [H-3]D-aspartate in neurons and astrocyteS (IC50 values 10-100 muM), DL-TBOA being slightly more potent than t-2,4-PDC. Release of preloaded [H-3]D-aspartate from neurons or astrocytes could be stimulated by addition of excess t-2,4-PDC whereas addition of DL-TBOA had no effect on [H-3]D-aspartate efflux. Moreover, DL-TBOA inhibited significantly the depolarization-induced (55 mM KCl) release of preloaded [H-3]D-aspartate in the neurons. The results reflect the fact that DL-TBOA is not transported by the glutamate carriers while t-2,4-PDC is a substrate which may heteroexchange with [H-3]D-aspartate. It is suggested that DL-TBOA may be used to selectively inhibit depolarization coupled glutamate release mediated by reversal of the carriers.
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