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Involvement of ERK phosphorylation in brainstem neurons in modulation of swallowing reflex in rats

机译:ERK磷酸化参与大鼠脑干神经元吞咽反射的调节

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摘要

In order to evaluate the neuronal mechanisms underlying functional abnormalities of swallowing in orofacial pain patients, this study investigated the effects of noxious orofacial stimulation on the swallowing reflex, phosphorylated extracellular signal-regulated kinase (pERK) and γ-aminobutyric acid (GABA) immunohistochemical features in brainstem neurons, and also analysed the effects of brainstem lesioning and of microinjection of GABA receptor agonist or antagonist into the nucleus tractus solitarii (NTS) on the swallowing reflex in anaesthetized rats. The swallowing reflex elicited by topical administration of distilled water to the pharyngolaryngeal region was inhibited after capsaicin injection into the facial (whisker pad) skin or lingual muscle. The capsaicin-induced inhibitory effect on the swallowing reflex was itself depressed after the intrathecal administration of MAPK kinase (MEK) inhibitor. No change in the capsaicin-induced inhibitory effect was observed after trigeminal spinal subnucleus caudalis lesioning, but the inhibitory effect was diminished by paratrigeminal nucleus (Pa5) lesioning. Many pERK-like immunoreactive neurons in the NTS showed GABA immunoreactivity. The local microinjection of the GABAA receptor agonist muscimol into the NTS produced a significant reduction in swallowing reflex, and the capsaicin-induced depression of the swallowing reflex was abolished by microinjection of the GABAA receptor antagonist bicuculline into the NTS. The present findings suggest that facial skin–NTS, lingual muscle–NTS and lingual muscle–Pa5–NTS pathways are involved in the modulation of swallowing reflex by facial and lingual pain, respectively, and that the activation of GABAergic NTS neurons is involved in the inhibition of the swallowing reflex following noxious stimulation of facial and intraoral structures.
机译:为了评估口面疼痛患者吞咽功能异常的潜在神经元机制,本研究调查了有害口咽刺激对吞咽反射,磷酸化细胞外信号调节激酶(pERK)和γ-氨基丁酸(GABA)免疫组化特征的影响还分析了脑干病变和向麻醉性孤束核(NTS)微注射GABA受体激动剂或拮抗剂对吞咽反射的影响。将辣椒素注射到面部(晶须垫)皮肤或舌肌后,抑制了向咽喉区域局部使用蒸馏水而引起的吞咽反射。鞘内注射MAPK激酶(MEK)抑制剂后,辣椒素对吞咽反射的抑制作用本身就降低了。三叉神经脊髓尾核损伤后,辣椒素诱导的抑制作用未见变化,但三叉神经旁核(Pa5)破坏使抑制作用减弱。 NTS中许多pERK样免疫反应性神经元均显示GABA免疫反应性。 GABAA受体激动剂麝香酚向NTS的局部显微注射导致吞咽反射显着降低,并且通过将GABAA受体拮抗剂双小分子显微注射至NTS消除了辣椒素诱导的吞咽反射抑制。目前的发现表明,面部皮肤-NTS,舌肌-NTS和舌肌-Pa5-NTS通路分别与吞咽反射有关,分别由面部和舌痛引起,而GABA能NTS神经元的激活与神经元的活化有关。有害刺激面部和口腔内结构后抑制吞咽反射。

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