This study explores the involvement of substance P (SP) in the parabrachial nucleus (PBN) and central amygdaloid nucleus (CeA) in the nociception–emotion link and of rats with masticatory myofascial pain (MMP) induced by chronic tetanic eccentric muscle contraction. A total of 18 rats were randomly and equally assigned for MMP (MMP group) and sham-MMP induction (sMMP group). MMP was induced by electrical-stimulated repetitive tetanic eccentric contraction of the masseter muscle for 14 consecutive days. Myofascial trigger points in the masseter muscle were identified by palpable taut bands, increased prevalence of endplate noise (EPN), focal hypoechoic nodules on ultrasound and restricted jaw opening. All animals were killed for morphological and SP immunohistochemical analyses. Chronic tetanic eccentric contraction induced significantly thicker masseter muscle confirmed by hypoechogenicity, increased prevalence and amplitudes of EPN, and limited jaw opening. Immunohistochemically, the SP-like positive neurons increased significantly in PBN and CeA of the MMP group. Our results suggested that MMP increases the SP protein levels in PBN and CeA, which play important roles in MMP-mediated chronic pain processing as well as MMP-related emotional processes.

这项研究探讨了P物质（SP）参与伤害性感受－情感联系的臂旁束核（PBN）和中央杏仁核（CeA）的参与以及慢性强直性肌偏心肌收缩引起的咀嚼性肌筋膜疼痛（MMP）的大鼠的参与。随机将18只大鼠平均分为MMP组（MMP组）和假MMP诱导组（sMMP组）。连续14天，通过电刺激咬肌的重复性强直性离心收缩来诱发MMP。咬肌中的肌筋膜触发点通过明显的拉紧带，端板噪声（EPN）的患病率增加，超声下局灶性低回声结节和下颌张开受限来识别。处死所有动物以进行形态学和SP免疫组织化学分析。慢性强直性离心收缩可引起咬肌明显增厚，这由低回声性，EPN的患病率和幅度增加以及颌骨张开受限所证实。免疫组织化学观察，MMP组的PBN和CeA中SP样阳性神经元显着增加。我们的结果表明，MMP增加了PBN和CeA中SP蛋白的水平，这在MMP介导的慢性疼痛过程以及MMP相关的情绪过程中起着重要作用。