After introducing potassium ion through the round window into the perilymphatic space of 40 guinea pigs by means of iontophoresis, physiological and histochemical investigations were performed to determine the role of the high perilymphatic potassium concentration in the vertiginous attack of Ménière's disease. About 15 min after the iontophoretic procedure, electronystagmography revealed irritative nystagmus for the first 5 min and then paralytic nystagmus for the following 6 to 24 hr. Histochemical analysis of the vestibular sensory epithelia revealed the increased activity of succinic dehydrogenase and Na-K-ATPase during irritative nystagmus and the decreased activity during paralytic nystagmus. The Na-K-ATPase activity was dominant in the synaptic area between the hair cells and the nerve-endings of the vestibular sensory epithelia. There was some delay between the reversal of nystagmus-direction and the change of enzyme activity. This delay was thought to be produced by the central regulatory mechanism for the disturbed tonus-balance in the vestibular nucleus. On the other hand, electrocochleography revealed the decrease of the action potential without any initial irritative cochlear sign, and the enzyme activity of the cochlear sensory cells was decreased from the beginning.
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