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首页> 外文期刊>Journal of Neurophysiology >Functional expression of α7-nicotinic acetylcholine receptors by muscle afferent neurons
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Functional expression of α7-nicotinic acetylcholine receptors by muscle afferent neurons

机译：肌肉传入神经元功能表达α7烟碱型乙酰胆碱受体

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摘要

The exercise pressor reflex (EPR) is generated by group III and IV muscle afferents during exercise to increase cardiovascular function. Muscle contraction is triggered by ACh, which is metabolized into choline that could serve as a signal of exercise-induced activity. We demonstrate that ACh can induce current in muscle afferents neurons isolated from male Sprague-Dawley rats. The nicotinic ACh receptors (nAChRs) appear to be expressed by some group III-IV neurons since capsaicin (TRPV1) and/or ATP (P2X) induced current in 56% of ACh-responsive neurons. ?- And ??-nAChRs have been shown to be expressed in sensory neurons. An ?-nAChR antibody stained 83% of muscle afferent neurons. Functional expression was demonstrated by using the specific ?-nAChR blockers ?conotoxin ImI (IMI) and methyllycaconitine (MLA). MLA inhibited ACh responses in 100% of muscle afferent neurons, whereas IMI inhibited ACh responses in 54% of neurons. Dihydro-?erythroidine, an ??-nAChR blocker, inhibited ACh responses in 50% of muscle afferent neurons, but recovery from block was not observed. Choline, an ?-nAChR agonist, elicited a response in 60% of ACh-responsive neurons. Finally, we demonstrated the expression of ?-nAChR by peripherin labeled (group IV) afferent fibers within gastrocnemius muscles. Some of these ?-nAChR-positive fibers were also positive for P2X3 receptors. Thus choline could serve as an activator of the EPR by opening ?-nAChR expressed by group IV (and possible group III) afferents. nAChRs could become pharmacological targets for suppressing the excessive EPR activation in patients with peripheral vascular disease.
机译：III和IV组肌肉传入运动产生运动加压反射（EPR），以增强心血管功能。肌肉收缩由ACh触发，ACh代谢为胆碱，可作为运动诱发活动的信号。我们证明ACh可以诱导从雄性Sprague-Dawley大鼠分离的肌肉传入神经元中的电流。烟碱型ACh受体（nAChRs）似乎由某些III-IV组神经元表达，因为辣椒素（TRPV1）和/或ATP（P2X）在56％的ACh反应性神经元中诱导电流。已经证明α-和β-nAChR在感觉神经元中表达。 α-nAChR抗体染色了83％的肌肉传入神经元。通过使用特定的β-nAChR阻滞剂βconotoxinImI（IMI）和甲基甘可尼丁（MLA）来证明功能性表达。 MLA抑制了100％的肌肉传入神经元的ACh反应，而IMI抑制了54％的神经元的ACh反应。 γ-nAChR阻滞剂二氢-赤藓类素抑制了50％的肌肉传入神经元的ACh反应，但未观察到从阻滞恢复。胆碱是一种α-nAChR激动剂，可引起60％的ACh反应神经元产生反应。最后，我们证明了腓肠肌内外周蛋白标记的（第IV组）传入纤维表达了β-nAChR。这些β-nAChR阳性纤维中的一些也对P2X3受体呈阳性。因此，胆碱可以通过打开由第IV组（和可能的第III组）传入的α-nAChR来充当EPR的激活剂。 nAChRs可能成为抑制外周血管疾病患者过度EPR活化的药理靶标。

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