Abstract
Electrophysiologic studies were performed to examine the effects of hypoxia on neuronal activities of the lateral vestibular and spinal trigeminal nuclei using rats anesthetized with chloral hydrate. The rats inhaled a gas mixture of 5% oxygen and 95% nitrogen for 3.5 minutes to induce hypoxia, followed by room air. Under these conditions, mean PaO2 was decreased from 85 to 22 mm Hg 3 minutes after the start of the inhalation concomitant with a decrease in blood pressure from 108 to 55 mm Hg. There were no significant differences in these variables between rats used for vestibular nucleus experiments and rats used for trigeminal nucleus experiments. In the lateral vestibular nucleus, hypoxia inhibited postsynaptic components of the evoked field potential, spike generation of monosynaptic neurons on vestibular nerve stimulation, and firing induced by iontophoretic application of glutamate. In the spinal trigeminal nucleus, however, there were no alterations of the field potential or spike generation of the neurons on trigeminal nerve stimulation. These results indicate that the lateral vestibular nucleus neurons are much more sensitive to hypoxia than the spinal trigeminal nucleus neurons. The failure of transmission in the monosynaptic neurons of the lateral vestibular nucleus is suggested to be due to the inhibition of excitability of the postsynaptic membrane.
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