Effects of anti-vertigo drugs on medial vestibular nucleus neurons activated by horizontal rotation.

Kawabata, Atsuhiko; Sasa, Masashi; Kishimoto, Takuzo; Takaori, Shuji

doi:10.1254/jjp.55.101

Cited by 16 publications

(3 citation statements)

References 14 publications

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“…Diphenidol has long been clinically deployed as an anti-emetic and anti-vertigo drug [5,6,12,13]. In the brain, the sites of action on the chemoreceptor trigger zone in the area postrema underlies its anti-emetic effect while its anti-vertigo effects are attributed to its actions on the vestibular apparatus [2].…”

Section: Introductionmentioning

confidence: 99%

“…There are few reports examining the direct effects of diphenidol on neurons or neuronal cell lines. In one study, diphenidol inhibited rotation-induced firing of feline medial vestibular nucleus type 1 neurons [5], but what specific neuronal receptors and ion channels diphenidol acted on were not elucidated. Diphenidol and its derivatives were shown to act as antagonists at the muscarinic receptors [15].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of voltage-gated K+ channels and Ca2+ channels by diphenidol

Leung

Wong

Cheng

et al. 2012

Pharmacological Reports

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Abstract:Background: Although diphenidol has long been deployed as an anti-emetic and anti-vertigo drug, its mechanism of action remains unclear. In particular, little is known as to how diphenidol affects neuronal ion channels. Recently, we showed that diphenidol blocked neuronal voltage-gated Na + channels, causing spinal blockade of motor function, proprioception and nociception in rats. In this work, we investigated whether diphenidol could also affect voltage-gated K + and Ca 2+ channels. Methods: Electrophysiological experiments were performed to study ion channel activities in two neuronal cell lines, namely, neuroblastoma N2A cells and differentiated NG108-15 cells. Results: Diphenidol inhibited voltage-gated K + channels and Ca 2+ channels, but did not affect store-operated Ca 2+ channels. Conclusion: Diphenidol is a non-specific inhibitor of voltage-gated ion channels in neuronal cells.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibition of voltage-gated K+ channels and Ca2+ channels by diphenidol

Leung

Wong

Cheng

et al. 2012

Pharmacological Reports

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“…The medial vestibular nucleus (MVN) neurons are classified into types I, II, III and IV, according to their responses to horizontal sinusoidal rotation (9)(10)(11). In brief, type I neurons exhibit an increase and a decrease in firing in response to horizontal rotations ipsilateral and contralateral to the recording site, respectively, while type II neurons show the opposite responses to type I neurons.…”

Section: Introductionmentioning

confidence: 99%

Enhancement of GABA-mediated Inhibition of Rat Medial Vestibular Nucleus Neurons by the Neurosteroid 20-Hydroxyecdysone

Okada

Ishihara²,

Sasa³

et al. 1998

Acta Oto-Laryngologica

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In vivo electrophysiological and patch-clamp studies were performed to determine whether 20-hydroxyecdysone (20-HE), a neurosteroid, influenced neuronal activities of the medial vestibular nucleus (MVN) using chloral hydrate-anesthetized rats and dissociated MVN neurons, respectively. Single neuronal activities of MVN were extracellularly recorded with a glass-insulated silver wire microelectrode attached along a seven-barreled micropipette. Each micropipette was filled with 20-HE, glutamate, bicuculline or 2 M NaCl. These chemicals were applied microiontophoretically to the immediate vicinity of the target neurons. Microiontophoretically applied 20-HE (20-80 nA) dose-dependently decreased rotation-induced firings of both type I and II neurons, which were identified according to their responses to horizontal sinusoidal rotations. Microiontophoretically applied bicuculline, a GABAA receptor antagonist, inhibited 20-HE-induced decreases in neuronal firing of MVN. These findings suggest that 20-HE potentiates the action of GABA, probably by acting directly on the GABAA receptor of MVN neurons. In addition, microiontophoretically applied 20-HE decreased firings induced by glutamate in both type I and II neurons. This decrease by 20-HE was also antagonized with bicuculline. Furthermore, the effects of 20-HE on GABA-induced currents in acutely dissociated MVN neurons were investigated using the whole-cell patch-clamp technique. Under voltage-clamp conditions, GABA (10 microM)-induced currents were potentiated in the presence of 20-HE (100 microM). These findings suggest that 20-HE inhibits MVN neurons by acting on the modulatory site on GABA receptor-ion channel complexes to potentiate GABA inhibition.

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Prednisolone excitation of medial vestibular nucleus neurons in cats

Yamanaka

Amano

Sasa

et al. 1995

Eur Arch Otorhinolaryngol

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An electrophysiological study was performed to determine whether prednisolone hydrochloride directly influenced neuronal activities of the medial vestibular nucleus (MVN) in alpha-chloralose-anesthetized cats. Single neuronal activities of MVN were recorded extracellularly with a glass-insulated silver wire microelectrode attached along a seven-barreled micropipette. Each barrel was filled with prednisolone, glutamate, glutamic acid diethylester (GDEE) or CoCl2. Except for prednisolone, which was administered both intravenously and microiontophoretically, other chemicals were applied microiontophoretically to the immediate vicinity of the target neurons. These MVN neurons were classified as type I and II neurons according to their responses to horizontal and sinusoidal rotations. Intravenous prednisolone (up to 5 mg/kg) enhanced spontaneous and rotation-induced neuronal firings of both type I and II neurons in a dose-dependent manner. In a similar tendency, microiontophoretically applied prednisolone (50-200 nA) dose-dependently increased spontaneous and rotation-induced firings of both type I and II neurons. Microiontophoretic GDEE, a non-selective glutamate receptor antagonist, inhibited glutamate- and rotation-induced neuronal discharges without affecting prednisolone-induced increases in neuronal responses of MVN. In addition, iontophoretically applied CoCl2, a Ca2+ channel blocker, did not affect prednisolone-, glutamate- and rotation-induced neuronal findings of MVN. These results suggest that prednisolone induces excitation of type I and II neurons, probably by acting directly on the membrane of MVN neurons. Thus, glucocorticoids such as prednisolone may be effective for the treatment of vertigo resulting from hypofunction of vestibular nucleus neurons.

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Effects of anti-vertigo drugs on medial vestibular nucleus neurons activated by horizontal rotation.

Cited by 16 publications

References 14 publications

Inhibition of voltage-gated K+ channels and Ca2+ channels by diphenidol

Inhibition of voltage-gated K+ channels and Ca2+ channels by diphenidol

Enhancement of GABA-mediated Inhibition of Rat Medial Vestibular Nucleus Neurons by the Neurosteroid 20-Hydroxyecdysone

Prednisolone excitation of medial vestibular nucleus neurons in cats

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