Plastic elimination of functional glutamate release sites by depolarization

Krista L. Moulder, Julian P. Meeks, Amanda A. Shute, Clair K. Hamilton, Gabriel De Erausquin, Steven Mennerick

Research output: Contribution to journalArticle

47 Scopus citations


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 pr, our results suggest the two can be independently manipulated. Selective depression of glutamate release may provide an adaptive mechanism by which neurons limit excitotoxicity.

Original languageEnglish (US)
Pages (from-to)423-435
Number of pages13
Issue number3
Publication statusPublished - May 13 2004


ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Moulder, K. L., Meeks, J. P., Shute, A. A., Hamilton, C. K., De Erausquin, G., & Mennerick, S. (2004). Plastic elimination of functional glutamate release sites by depolarization. Neuron, 42(3), 423-435.