Regulation of the activity and cell surface expression of the neuronal glutamate transporter EAAC1 by multiple signaling pathways

TL;DRAbstract

The primary mechanism for the removal of glutamate and aspartate from the extracellular space is a family of five sodium-dependent high affinity transporters. These transporters are selectively expressed in either neurons or glia, and may be critical for the limitation of excitotoxic injury following acute insults to the CNS. The neuronal transporter EAAC1 is of special interest because it is enriched in the hippocampus and cortex, two areas exquisitely sensitive to excitotoxic insults. In C6 glioma, a CNS-derived cell line that endogenously and selectively expresses the EAAC1 subtype of transporter, L-[ 3H]-glutamate transport activity was rapidly increased following phorbol 12-myristate 13-acetate (PMA)-induced activation of protein kinase C (PKC). This increase was correlated with an increase in cell surface EAAC1 immunoreactivity as measured by cell surface biotinylation, followed by batch extraction and Western blotting. The effects of PMA occurred within minutes and did not chang

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