The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.
Mechanism of glutamate release from rat hippocampal slices during in vitro ischemia.
There was a large release of endogenous glutamate and of pre-accumulated [3H]-D-aspartate from rat hippocampal slices during deprivation of oxygen and glucose ( in vitro ischemia). The role of Na(+)-dependent glutamate transporters in this process was investigated. The release of both glutamate and [3H]-D-aspartate was largely blocked by two competitive substrate analogues of the Na(+)-dependent glutamate transporters (L-trans-pyrrolidine-2,4-dicarboxylate and D,L-threo-B-hydroxyaspartate) if the substrate analogues were intracellularly loaded prior to the ischemia. The pre-loaded analogue, D,L-threo-B-hydroxyaspartate, did not block exocytotic release of glutamate, induced by high-potassium. Dihydrokainate, an inhibitor of a subset of the Na(+)-dependent transporters, did not inhibit ischemia-induced release of glutamate or [3H]-D-aspartate. However, it did block release induced by veratridine, which was also blocked by the pre-loaded substrate analogues. Dihydrokainate could still inhibit veratridine-induced release during ischemia, showing that conditions during ischemia did not reduce its efficacy. It is concluded that release of glutamate during ischemia is largely via reversal of the Na(+)-dependent glutamate transport system. The differential effects of dihydrokainate and the competitive substrate analogues on ischemia-induced release indicate that this release occurs via a subset of the glutamate transporters that are present in the hippocampus.[1]References
- Mechanism of glutamate release from rat hippocampal slices during in vitro ischemia. Roettger, V., Lipton, P. Neuroscience (1996)
