Redox modulation of N-methyl-D-aspartate-stimulated neurotransmitter release from rat brain slices.
Redox modulation of N-methyl-D-aspartate-stimulated neurotransmitter release from rat brain slices.
复制标题
N-甲基-D-天冬氨酸刺激的大鼠脑切片神经递质释放的氧化还原调节。
DOI：
10.1111/j.1471-4159.1991.tb06422.x
复制
发表时间：
1991
影响因子：
4.7
通讯作者：
Blair,R
中科院分区：
文献类型：
--
作者：
Woodward,JJ;Blair,R
Rat brain cortical slices released tritiated norepi‐nephrine ([3H]NA) during a 2‐min stimulation withN‐methyl‐d‐aspartate (NMDA). Dithiothreitol (DTT; 0.1–5 mM), present for 6 min prior to stimulation, dose‐depen‐dently increased the release of [3H]NA from cortical slices stimulated with a maximally effective concentration of NMDA (500μM). Similar results were observed for [3H]NA release from hippocampal slices and tritiated and endogenous dopamine release from striatal slices. DTT treatment also markedly shifted the dose‐response curve of NMDA to the left. Cortical slices released approximately the same amount of [JH]NA with 10μMNMDA following DTT treatment (about 5%) as non‐DTT‐treated control slices did with 500 μMNMDA. The effects of DTT were fully reversed by subsequent treatment with 5,5′‐dithio‐bis(2‐nitrobenzoic acid) (DTNB; 0.5 mM). DTT treatment did not significantly alter the ability of magnesium (1.3 mM) or the polyamine antagonist arcaine to block the NMDA‐stimulated release of [3H]NA. In contrast, DTT treatment significantly attenuated the antagonist effects of the competitive glycine antagonist, 7‐chlorokynurenic acid, and the competitive NMDA antagonist, 2‐aminophosphonopentanoic acid. These results suggest that oxidation and reduction of disulfide bonds located within the NMDA receptor complex might regulate the activation of the NMDA receptor. This could have important consequences in vivo if endogenous oxidizing/reducing systems are found to have similar effects on NMDA‐stimulated responses.
