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.
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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
Lust,WD
中科院分区:
医学3区
文献类型:
--
作者:
Whittingham,TS;Assaf,H;Selman,WR;Ratcheson,RA;Lust,WD

文献摘要

相似文献

当浓度超过 1 mM 时,将外源性谷氨酸引入正常呼吸的海马切片会导致 ATP、磷酸肌酸 (PCr) 和细胞内 pH (pHi) 大幅降低。添加 MK-801(一种 NMDA 受体拮抗剂)并不能阻止这些变化,NMDA 或高钾也不能模拟这些变化。此外,添加天冬氨酸-b-羟酸盐或用胆碱替代钠并不能阻止谷氨酸诱导的代谢改变,这两者都会抑制高亲和力钠依赖性谷氨酸的吸收。这些结果表明,即使葡萄糖和氧气维持在控制水平,单独的谷氨酸也可以在神经组织中产生显着的能量应激。并且能量应激似乎不是由 NMDA 诱导的去极化或谷氨酸的高亲和力摄取特异性介导的。
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.