Glutamate-induced energetic stress in hippocampal slices: Evidence against NMDA and glutamate uptake as mediators

Autor: Whittingham, Tim S., Assaf, Hussein, Selman, Warren R., Ratcheson, Robert A., Lust, W. David
Zdroj: Metabolic Brain Disease; June 1992, Vol. 7 Issue: 2 p77-92, 16p
Abstrakt: The introduction of exogenous glutamate to normally respiring hippocampal slices produced substantial reductions in ATP, phosphocreatine (PCr) and intracellular pH (pHi) when the concentration exceeded 1 mM. These changes were not prevented by addition of MK-801 (an NMDA receptor antagonist), nor were they mimicked by NMDA or high potassium. In addition, the glutamate-induced metabolic alterations were not prevented by addition of aspartate-b-hydroxymate or sodium substitution by choline, both of which should inhibit high-affinity sodium-dependent glutamate uptake. These results suggest that glutamate alone can produce marked energetic stress in neural tissue, even when glucose and oxygen are maintained at control levels; and that the energetic stress does not appear to be specifically mediated by NMDA-induced depolarization, or by high-affinity uptake of glutamate.
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