Hypoxia-induced electrical changes in striatal neurons.
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.
Calabresi
P
P
Clinical Neurologica, Dip. Sanità, Università di Roma Tor Vergata, Italy.
Pisani
A
A
Mercuri
N B
NB
Bernardi
G
G
D000818:Animals; D003342:Corpus Striatum / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D002534:Hypoxia, Brain / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D010042:Ouabain / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D009435:Synaptic Transmission / Q000187:drug effects; D013779:Tetrodotoxin / Q000494:pharmacology
D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D013779:Tetrodotoxin; D010042:Ouabain