Journal
NEURON
Volume 42, Issue 3, Pages 423-435Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(04)00184-9
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Funding
- NIAAA NIH HHS [AA 12592] Funding Source: Medline
- NIDA NIH HHS [1F32 DA 15948, 5T32 DA 07261] Funding Source: Medline
- NINDS NIH HHS [NS 40488] Funding Source: Medline
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To examine persisting effects of depolarizing rises in extracellular potassium concentration ([K+](o)) on synapses, we depolarized cells to simulate ischemia-like rises in [K+](o). Elevated [K+](o) for 1-16 hr severely depressed glutamate signaling, while mildly depressing GABA transmission. The glutamate-specific changes were plastic over several hours and involved a decrease in the size of the pool of releasable vesicles. Rather than a reduction of the number of vesicles per release site, the change involved functional elimination of release sites. This change was clearly dissociable from a second effect, depressed probability of transmitter release, which was common to both glutamate and GABA transmission. Thus, while other recent evidence links alteration of the releasable pool size with changes in p(r), our results suggest the two can be independently manipulated. Selective depression of glutamate release may provide an adaptive mechanism by which neurons limit excitotoxicity.
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