Abstract
It is well known that anticholinergic agents such as atropine and scopolamine are effective as anti-motion sickness drugs, however, the mechanism of action in the vestibular system is inadequately understood. It has been demonstrated by several investigators (1-5) that neurons in the vestibular nucleus are excited by local application of acetylcholine. Gerebtzoff (6) has shown a histochemical localization of cholinesterase in the vestibular nucleus of cats. Contents of the enzyme were relatively high in the superior and lateral parts of the nucleus, but low in the medial and inferior parts. According to the hypothesis of Wood and Graybiel (7), motion sickness occurred when activation of the central cholinergic system disturbed the balance of vestibular reactions, and protection would be achieved by utilizing anticholinergic drugs. Diphenidol (1, 1-diphenil-4-piperidine-1-butanol) which is related chemically to trihexylphenidil and chlorphenianol has been found effective in the treatment of motion sickness (8-11). Leonard et al. (12) have shown that diphenidol is equal in anti-emetic potency to chlorpromazine and that diphenidol has a greater selectivity of pharmacological action in experimental animals. The present experiments using cats were designed to study the effects of diphenidol on evoked responses in the central vestibular and visual systems.
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