Ischemia-induced changes in evoked glutamate release can be reduced by calcium buffering in hippocampal CA1 region.
Published: 2006
Language: eng
Number of pages: 96
ISBN-13: 9780494213179
Description: Oxygen-glucose deprivation (OGD) leads to the depression of evoked excitatory post-synaptic potentials (fEPSPs) and an increase in spontaneous miniature EPSPs (mEPSPs). We hypothesized that application of cell-permeant calcium chelators will reverse the OGD-induced depression of fEPSPs and promote better recovery of synaptic transmission.Tissue pre-incubated in BAPTA-AM, EGTA-AM or controls was exposed to OGD (glucose-free medium aerated with 95% N2- 5% CO2) for 2, 4, or 6 minutes. OGD depressed fEPSPs and increased mEPSP frequency, recorded from hippocampal CA1 region. Some depression of fEPSPs remained after administration of a selective adenosine A1 antagonist. BAPTA-AM, but not EGTA-AM, depressed fEPSPs in control perfusate by 48 +/- 8%. Both chelators partly prevented the ischemia-induced depression of fEPSPs and promoted faster recovery from ischemia. Data suggest that intracellular Ca2+ regulation is altered early on in ischemia and that cell-permeant calcium chelators may prevent some ischemia-induced changes in neurotransmitter release and promote better recovery.
Notes: Source: Masters Abstracts International, Volume: 45-03, page: 1396.

Thesis (M.Sc.)--University of Toronto, 2006.

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