舌神經衝動對咬肌神經刺激在大白鼠視丘腹後內核誘發電位之突觸前抑制作用
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Date
1997-12-??
Authors
董明倫
林金盾
吳京一
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Journal ISSN
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Publisher
國立臺灣師範大學生命科學學系
Department of Life Science, NTNU
Department of Life Science, NTNU
Abstract
視丘腹後內核（VPM）為三叉神經丘腦徑的特殊主要傳遞神經核；它接受負責開口及閉口協調作用的三叉神經脊髓路核（NTST）傳入神經衝動。以刺激舌神經為條件刺激，觀察其對咬肌神經在VPM上誘發電位之影響。結果觀察到在早期的作用時間途徑有明顯的抑制作用；其持續的時間約200 ms 。以procaine 滴於舌神經上阻斷其神經傳導，則舌神經之條件刺激對咬肌神經在VPM上誘發之抑制作用不再發生。以直流電破壞NTST之吻部使部份舌神經之神經衝動無法傳遞至VPM，結果咬肌神經在VPM中誘發電位之抑制作用會減少。由股靜脈分別注入strychnine或 picrotoxin，觀察藥物對舌神經條件刺激作用的影響，發現strychnine使得抑制作用更為明顯，而picrotoxin則減少了抑制作用，故推測舌神經對於咬肌神經在VPM中誘發電位之抑制作用為突觸前抑制。
The thalamic ventral posteromedial nucleus (VPM) is main relay nucleus of the trigemino-thalamic tract. VPM can accept afferent impulses from the nucleus of spinal tract of trigeminal nerve (NTST) that integrates jaw-closing and -opening movement. The evoked potentials of the masseteric nerve on the contralateral VPM were depressed by the conditioning stimuli of the lingual nerve. A monophasic suppression was observed at the early period of the time course. When procaine was applied on the lingual nerve to block the conduction of nerve impulses, the suppression of the evoked potential of the masseteric nerve on the contralateral VPM induced by the lingual nerve disappeared. When the rostral part of NTST was lesioned by the direct current, the suppression was decreased. On the other hand, the suppression was increased after intravenous administration of strychnine but was decreased by picrotoxin. It is suggested that the suppression of the evoked potentials of the masseteric nerve on the contralateral VPM induced by the lingual nerve is caused by presynaptic inhibition.
The thalamic ventral posteromedial nucleus (VPM) is main relay nucleus of the trigemino-thalamic tract. VPM can accept afferent impulses from the nucleus of spinal tract of trigeminal nerve (NTST) that integrates jaw-closing and -opening movement. The evoked potentials of the masseteric nerve on the contralateral VPM were depressed by the conditioning stimuli of the lingual nerve. A monophasic suppression was observed at the early period of the time course. When procaine was applied on the lingual nerve to block the conduction of nerve impulses, the suppression of the evoked potential of the masseteric nerve on the contralateral VPM induced by the lingual nerve disappeared. When the rostral part of NTST was lesioned by the direct current, the suppression was decreased. On the other hand, the suppression was increased after intravenous administration of strychnine but was decreased by picrotoxin. It is suggested that the suppression of the evoked potentials of the masseteric nerve on the contralateral VPM induced by the lingual nerve is caused by presynaptic inhibition.