Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.
Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.
Neuropharmacology. 2020 Sep 15;175:108197. doi: 10.1016/j.neuropharm.2020.108197. Epub 2020 Jun 13.
Temporomandibular Disorder (TMD) patients report amplification of pain in the masticatory muscles after psychological trauma or stressful conditions. The mechanisms underlying this phenomenon are yet to be elucidated. This study combined immunohistochemistry with single cell in vivo electrophysiology recordings of masticatory muscle afferent fibers to investigate the role of α-adrenergic receptors in muscle nociception. It was found that a subset of trigeminal afferent fibers which innervate the masseter and temporal muscles expressed α, α and α receptors, including a smaller number of putative nociceptors which co-expressed TrpV receptors. Local injection of the selective α adrenergic receptor agonist phenylephrine into masticatory muscle decreased and increased the mechanical activation threshold of slow and fast conducting afferent fibers, respectively. This effect was reversed by co-administration of the α selective antagonist terazosin. To rule out the possibility that local ischemia was responsible for the observed effect of phenylephrine on masticatory muscle afferent fibers, additional experiments were conducted where blood flow to the masticatory muscle was reduced by common carotid artery occlusion. This investigation found that muscle blood flow occlusion increased the mechanical activation threshold of the majority of masticatory muscle afferent fibers unrelated to conduction velocity. These findings suggest that under conditions of increased sympathetic tone, such as those related to stress, noradrenaline may sensitize masticatory muscle nociceptors to increase pain and desensitize muscle proprioceptors to alter muscle tone, through activation of α receptors.
颞下颌关节紊乱（TMD）患者报告在心理创伤或应激状态后咀嚼肌疼痛加剧。目前尚不清楚这种现象的发生机制。本研究结合免疫组织化学和咀嚼肌传入纤维的单细胞活体电生理学记录，探讨了α-肾上腺素能受体在肌肉伤害感受中的作用。结果发现，支配咀嚼肌的三叉神经传入纤维中存在α、α和α受体亚群，其中包括数量较少的可能同时表达 TrpV 受体的伤害感受器。将选择性α肾上腺素能受体激动剂苯肾上腺素局部注射到咀嚼肌中，分别降低和增加慢和快传导传入纤维的机械激活阈值。该效应可被α选择性拮抗剂特拉唑嗪逆转。为了排除苯肾上腺素对咀嚼肌传入纤维的观察效应是由于局部缺血引起的可能性，进行了额外的实验，其中通过颈总动脉闭塞来减少咀嚼肌的血流。这项研究发现，肌肉血流闭塞增加了大多数与传导速度无关的咀嚼肌传入纤维的机械激活阈值。这些发现表明，在交感神经张力增加的情况下，例如与压力相关的情况，去甲肾上腺素可能通过激活α受体使咀嚼肌伤害感受器敏感化，从而增加疼痛，并使肌肉本体感受器脱敏，改变肌肉张力。
