HYPOXIA-INDUCED ELECTRICAL CHANGES IN STRIATAL NEURONS

被引:18
|
作者
CALABRESI, P [1 ]
PISANI, A [1 ]
MERCURI, NB [1 ]
BERNARDI, G [1 ]
机构
[1] IRCCS, ROME, ITALY
来源
关键词
EXCITATORY AMINO ACIDS; HYPOXIA; ISCHEMIA; SODIUM-POTASSIUM; ATP-DEPENDENT PUMP; STRIATUM; SYNAPTIC TRANSMISSION;
D O I
10.1038/jcbfm.1995.142
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We have studied the effects of hypoxia on the membrane properties of striatal neurons intracellularly recorded from a corticostriatal slice preparation. Brief (2-10 min) periods of hypoxia produced reversible membrane depolarizations. Longer periods of hypoxia (12-20 min) produced irreversible membrane depolarizations. In voltage-clamp experiments, hypoxia caused an inward current coupled with an increased membrane conductance. Tetrodotoxin or low calcium (Ca2+)-high magnesium-containing solutions blocked synaptic transmission, but they did not reduce the hypoxia-induced electrical changes. Antagonists of excitatory amino acid (EAA) receptors failed to affect the electrical effects caused by oxygen (O-2) deprivation. In low sodium (Na+)-containing solutions the hypoxia-induced inward current was largely reduced. Blockade of ATP-dependent Na+-potassium (K+) pump by ouabain enhanced hypoxia-induced membrane depolarizations and/or inward currents. Our findings indicate that, at least for in vitro experiments, the release of EAAs is not required for the acute hypoxia-induced electrical changes in striatal neurons.
引用
收藏
页码:1141 / 1145
页数:5
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