Masseter muscle contraction and cervical muscle sensitization by nerve growth factor cause mechanical hyperalgesia in masticatory muscle with activation of the trigemino-lateral parabrachial nucleus system in female rats
Masseter muscle contraction and cervical muscle sensitization by nerve growth factor cause mechanical hyperalgesia in masticatory muscle with activation of the trigemino-lateral parabrachial nucleus system in female rats
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DOI：
10.1111/head.14406
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发表时间：
2022-11-02
期刊：
影响因子：
5
通讯作者：
Mizumura，Kazue
中科院分区：
文献类型：
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作者：
Kubo，Asako;Sugawara，Shiori;Mizumura，Kazue
目的建立一种新的大鼠颅面肌痛模型，并阐明该模型中哪些中枢神经系统通路被激活。疼痛被认为是一种多因素疾病，有几个共存的原因。据我们所知，有没有多种类型的stimulations.MethodsWe颅面肌痛觉过敏所造成的模型注射到雌性和雄性大鼠的咬肌和反复电刺激咬肌（MM）10天。我们确定了MM的机械头回缩阈值和下脑干不同区域磷酸化细胞外信号相关激酶1/2（pERK）免疫反应性的程度。我们进行了逆行追踪，以确定机械敏感性MM-支配的次级神经元的投射到臂旁外侧核。最后，我们给大鼠吗啡，以确定是否增加pERK免疫反应依赖于有害inputs.ResultsIn雌性大鼠，但不是雄性大鼠，机械头回缩阈值显着下降，从第9天至12。与其他单一刺激组的大鼠相比，两种刺激组雌性大鼠脑干中pERK免疫反应性神经元的数量显著增加。脑干中的机械敏感性MM神经支配神经元投射到臂旁核。吗啡给药阻断了pERK免疫反应阳性神经元数量的增加，在脑干和臂旁nucleus.ConclusionsWe建立了颅面肌痛模型相结合，在雌性大鼠的Escherzius和MM刺激。我们发现MM的机械性痛觉过敏和从脑干到臂旁核的疼痛通路的激活。该模型反映了颅面肌痛患者的特点，可能有助于阐明这些疾病的致病机制。
ObjectiveTo establish a new rat model of craniofacial myalgia, and to clarify which central nervous system pathways are activated in the model.BackgroundCraniofacial myalgia, represented by myogenous temporomandibular disorder and tension‐type headache with pericranial tenderness, is more common in female patients. The pain is thought to be a type of multifactorial disorder with several coexisting causes. To our knowledge, there are no models of craniofacial muscle hyperalgesia caused by multiple types of stimuli.MethodsWe injected nerve growth factor into the trapezius muscle of female and male rats and repeatedly stimulated the masseter muscle (MM) electrically for 10 days. We determined the mechanical head‐withdrawal threshold of MM and extent of phosphorylated extracellular signal‐related kinase 1/2 (pERK) immunoreactivity in various regions of the lower brainstem. We conducted retrograde tract‐tracing to determine the projection of mechanosensitive MM‐innervating secondary neurons to the lateral parabrachial nucleus. Finally, we administered morphine in rats to determine whether increases of pERK immunoreactivity were dependent on noxious inputs.ResultsIn female rats, but not male rats, the mechanical head‐withdrawal threshold was decreased significantly from days 9 to 12. The number of pERK‐immunoreactive neurons in the brainstem was increased significantly in female rats in the group with both stimuli compared to rats in other groups with a single stimulus. Mechanosensitive MM‐innervating neurons in the brainstem projected to the parabrachial nucleus. Morphine administration blocked the increase in the number of pERK‐immunoreactive neurons in both the brainstem and parabrachial nucleus.ConclusionsWe established a model of craniofacial myalgia by combining trapezius and MM stimuli in female rats. We found mechanical hyperalgesia of the MM and activation of the pain pathway from the brainstem to parabrachial nucleus. The model reflects the characteristics of patients with craniofacial myalgia and might be helpful to clarify the pathogenic mechanisms underlying these disorders.