ネコ前庭神経外側核への中枢内入力系に関するＨＲＰおよび電気生理学的研究 特にオリーブ核‐前庭神経外側核系について

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Central projections to the lateral vestibular nucleus (LVN) in cats were examined using a retrograde transport of horseradish peroxidase (HRP). Furthermore, electrophysiological studies were performed to elucidate the influence of the inferior olivary nucleus (IO) on the LVN neuron and possible neurotransmitters involved in the transmission from the IO to the LVN using the microiontophoretic technique. When HRP was microiontophoretically applied to the immediate vicinity of the LVN neuron, which was monosynaptically activated by vestibular nerve stimulation, HRP-labeled cells were found in the following areas: bilateral fastigial, bilateral dentate and ipsilateral interpositus nuclei of cerebellum; bilateral medial, bilateral descending and contralateral lateral vestibular nuclei; bilateral gigantocellular and ipsilateral lateral reticular nuclei; and contralateral dorsal cap and β nucleus of the IO. HRP-labeled Purkinje cells were observed in the ipsilateral cerebellar nodulus, ligula and flocculus. Effects of IO stimulation were examined on 168 LVN neurons monosynaptically elicited by vestibular nerve stimulation using decerebellate cats anesthetized with α-chloralose. Forty-three neurons were monosynaptically activated by IO stimulation and excitatory responses were dose-dependently inhibited with iontophoretic application of atropine, an anticholinergic drug. The conditioning stimulus to the IO preceding the test stimulus to the vestibular nerve inhibited the orthodromic spike upon the test stimulation in 22 neurons and the inhibition was antagonized with iontophoretic application of bicuculline, a GABA antagonist. In 9 LVN neurons, IO stimulation produced an antidromic spike. Histological examination showed that excitatory and/or inhibitory effects on the LVN neurons were observed when the stimulus was applied to the dorsal cap and/or β nucleus of the contralateral IO. These results suggest that the LVN neurons monosynaptically activated by vestibular nerve stimulation receive both excitatory input mediated by acetylcholine and inhibitory effect mediated by GABA from the contralateral dorsal cap and β nucleus of the IO.