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巨细胞网状核在被盖脚桥核刺激期间抑制吞咽反射中的作用

Role of the gigantocellular reticular nucleus in suppression of the swallowing reflex during stimulation of the pedunculopontine tegmental nucleus.

基础研究咽喉科IF 2.6Q2

文献信息

中文摘要

目的: 既往研究报道,刺激被盖脚桥核(PTg)和巨细胞网状核(Gi)分别抑制和调节吞咽反射。吞咽中枢模式发生器包括孤束核(Sol)和外侧网状结构(LRF)。PTg投射至Gi,而Gi投射至Sol和LRF。因此,提示PTg诱导的吞咽反射抑制是通过Gi介导的。我们研究了Gi的电毁损,或将甲基牛扁亭碱(MLA)——一种α7烟碱型乙酰胆碱受体拮抗剂——微量注射到Gi中,是否影响PTg诱导的吞咽反射抑制。
方法: 实验在氨基甲酸乙酯麻醉的大鼠上进行。通过反复电刺激喉上神经诱发吞咽反射,并使用肌电图从下颌舌骨肌记录反应。对PTg进行电刺激。在确认PTg诱导的吞咽反射抑制后,进行Gi的电毁损或将MLA注射到Gi中。
结果: Gi的电毁损或将MLA注射到Gi中均可减少PTg诱导的首次吞咽起始潜伏期延长。
结论: 这些结果提示,刺激PTg诱导的首次吞咽起始潜伏期延长是通过Gi中继介导的。

英文摘要

OBJECTIVES: A previous study reported that stimulation of the pedunculopontine tegmental nucleus (PTg) and the gigantocellular reticular nucleus (Gi) suppressed and modulated the swallowing reflex, respectively. The swallowing central pattern generator comprises the nucleus of the solitary tract (Sol) and lateral reticular formation (LRF). The PTg projects to the Gi, and the Gi projects to the Sol and LRF. Thus, suggesting that PTg-induced suppression of the swallowing reflex is mediated via the Gi. We investigated whether electric lesions of the Gi, or microinjection of methyllycaconitine (MLA), -an α7 nicotinic acetylcholine receptor antagonist, -into the Gi, affect PTg-induced suppression of the swallowing reflex.
METHODS: Experiments were performed on urethane-anesthetized rats. The swallowing reflex was evoked by repetitive electrical stimulation of the superior laryngeal nerve, and responses were recorded from the mylohyoid muscle using electromyography. The PTg was stimulated electrically. Following confirmation of PTg-induced suppression of the swallowing reflex, electric lesions of the Gi or injection of MLA into the Gi were performed.
RESULTS: Electric lesions of the Gi or injection of MLA into the Gi each reduced PTg-induced prolongation of the onset latency of the first swallow.
CONCLUSIONS: These results suggest that prolongation of the onset latency of the first swallow, induced by stimulation of the PTg, is mediated by a relay through the Gi.