Abstract
To elucidate the effectiveness of the drug in the treatment of vertebrobasilar insufficiency (VBI), we performed an electrophysiological study to examine the effects of ipenoxazone hydrochloride, a glutamate blocker, on hypoxia-induced firing in the medial vestibular nucleus (MVN) neuron, using alpha-chloralose-anesthetized cats. The single neuronal activity of the MVN was recorded extracellularly with a glass-insulated silver wire microelectrode attached along a seven-barrel micropipette. The firing rate of MVN neurons showed a transient increase [hypoxic depolarization (HD)] during 5% O(2) inhalation, followed by a gradual decrease and disappearance. HD and the time to disappearance of firing induced by hypoxia were inhibited by iontophoretic application of ipenoxazone hydrochloride. These results suggest that ipenoxazone hydrochloride protects against hypoxic neuronal dysfunction, and may be an effective drug for vertigo caused by VBI.
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