Glutamate-induced energetic stress in hippocampal slices: evidence against NMDA and glutamate uptake as mediators.
Glutamate-induced energetic stress in hippocampal slices: evidence against NMDA and glutamate uptake as mediators.
复制标题
海马切片中谷氨酸诱导的能量应激:反对 NMDA 和谷氨酸摄取作为介质的证据。
DOI:
10.1007/bf01000147
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发表时间:
1992
影响因子:
3.6
通讯作者:
Lust,WD
中科院分区:
文献类型:
--
作者:
Whittingham,TS;Assaf,H;Selman,WR;Ratcheson,RA;Lust,WD
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.