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- 山中 敏彰
- 奈良県立医科大学耳鼻咽喉科学教室
書誌事項
- タイトル別名
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- Excitatory Effects of Glucocorticoids on Neuronal Activity in the Medial Vestibular Nucleus. Mediation by Glucocorticoid Receptor on the Membrane.
- MEDIATION BY GLUCOCORTICOID RECEPTOR ON THE MEMBRANE
- グルココルチコイド膜レセプターを介する作用を中心に
この論文をさがす
抄録
Although glucocorticoids are sometimes used for the treatment of vertigo in certain disorders such as Meniere's disease, the mechanism underlying anti-vertigo effect remains unknown. The present study was performed to examine the effects of a glucocorticoid, dexamethasone, on neuronal activity in the medial vestibular nucleus (MVN) to determine whether or not the drug acts directly on the MVN neuron using α-chloralose-anesthetized cats which were fixed in a stereotaxic instrument placed on a turn-table. Single neuronal activities in the MVN were extracellularly recorded with a glass-insulated silver wire microelectrode attached along a seven-barreled micropipette. Each pipette was filled with dexamethasone phosphate (0.1M), monosodium glutamate (1M), glutamic acid diethylester (GDEE) (0.05M: a non-selective glutamate receptor antagonist), CoC12, (0.1M: a non-specific calcium channel blocker), RU38486 (0.01M: glucocorticoid receptor antagonist) or potassium canrenoate (0.1M: a mineralcorticoid receptor antagonist). These chemicals were microiontophoretically applied to the immediate vicinity of the target neuron being recorded. The effects of the drugs were examined on type I neurons which were identified according to responses to rotation: the neuron showed an increase and a decrease in firing with ipsilateral and contralateral rotation to the recording site, respectively. Microiontophoretically applied dexamethasone (50-200nA) dose-dependently increased spontaneous firing of<br>MVN neurons. However iontophoretic application of GDEE did not affect the dexamethasoneinduced increase in firing of the MVN neurons but inhibited glutamate-and rotation-induced firing. Microiontophoretically applied Co2+ did not affect dexamethasone-, glutamate-and rotationinduced firing. However, dexamethasone-induced firing was dose-dependently suppressed by iontophoretic RU38486, but not by canrenoate. Then a microdialysis study using α-chloraloseanesthetized cats was performed to determine whether or not dexamethasone affects the release of glutamate from vestibular nerve terminals. The microdialysis probe (CMA/10, 2mm) was inserted into the MVN and perfused with Ringer solution at 2ml/min. Samples were collected at 10-min intervals. Endogeneous glutamate was measured using the HPLC-ECD method. When repetitive stimuli (200μsec duration, 0.5mA and 5Hz) were given to the vestibular nerve for 10 min, an increase in the release of glutamate was observed. Dexamethasone did not produce spontaneous or stimulation-induced release of glutamate. These results suggest that dexamethasone acts directly on the MVN neuron to excite neuronal activity through glucocorticoid receptors on neuron membranes, but the excitation is not due to the release of glutamate.
収録刊行物
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- 日本耳鼻咽喉科学会会報
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日本耳鼻咽喉科学会会報 97 (5), 855-867, 1994
一般社団法人 日本耳鼻咽喉科頭頸部外科学会