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 (O2) 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.

Hypoxia-induced electrical changes in striatal neurons

Pisani A;
1995

Abstract

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 (O2) 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.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11571/1353475
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