1 Center for Oral and Jaw Functional Diagnosis, Treatment and Research, Department of Prosthodontics, Peking University School and Hospital of Stomatology & National Engineering Laboratory for Digital and Material Technology of Stomatology & Beijing Key Laboratory of Digital Stomatology, Beijing, China.
J Dent Res. 2019 May;98(5):589-596. doi: 10.1177/0022034519827590. Epub 2019 Feb 20.
Acute occlusal interference following improper occlusal alteration in dental practice can induce chronic masticatory muscle pain. The underlying mechanism has not been clarified. Synaptic plasticity in the anterior cingulate cortex (ACC) plays a key role in the chronic pain state. This study investigated the role of synaptic plasticity in the ACC in acute occlusal interference-induced chronic masticatory muscle pain. A rat model of experimental occlusal interference (EOI) was established. In vivo local field potential (LFP) recording was conducted to evaluate the change of synaptic strength and plasticity from the medial thalamus (MT) to the ACC after EOI application. The effects of microdialysis of antagonists of glutamate receptors into the ACC on synaptic transmission from the MT to the ACC were examined. Furthermore, the influence of inhibiting glutamate receptors in the ACC on EOI-induced mechanical hyperalgesia in the masseter muscles of rats was investigated. The amplitude of LFP in the ACC evoked by MT stimulation was significantly potentiated since 14 d of EOI application. Long-term potentiation of LFP in the ACC was reliably induced by theta burst stimulation to the MT in control rats but was occluded in 14-d EOI rats. Microdialysis of AMPA/kainate receptor antagonist CNQX into the ACC attenuated LFP in the ACC evoked by stimulating the MT in control and EOI rats. Administration of NMDA receptor subunit NR2B antagonist Ro 25-6981 into the ACC significantly alleviated the potentiation of MT stimulation-evoked LFP in the ACC of EOI rats without affecting that in control rats. EOI-induced hyperalgesia in the bilateral masseter muscles of rats was dose-dependently relieved after microdialysis of Ro 25-6981 into ACC. These findings provide direct evidence that prolonged acute occlusal interference potentiates synaptic transmission in the ACC, which in turn mediates chronic masticatory muscle pain.
牙体预备中不合适的咬合改变会导致急性咬合干扰，进而引起慢性咀嚼肌疼痛。其潜在机制尚未阐明。扣带回前部皮层（ACC）中的突触可塑性在慢性疼痛状态中起着关键作用。本研究旨在探讨 ACC 中的突触可塑性在急性咬合干扰诱导的慢性咀嚼肌疼痛中的作用。建立了实验性咬合干扰（EOI）大鼠模型。通过对内侧丘脑（MT）至 ACC 的电生理记录，评估 EOI 应用后突触强度和可塑性的变化。观察将谷氨酸受体拮抗剂微透析至 ACC 对 MT 至 ACC 的突触传递的影响。此外，还研究了抑制 ACC 中的谷氨酸受体对 EOI 诱导的大鼠咬肌机械性痛觉过敏的影响。自 EOI 应用 14 天后，ACC 中由 MT 刺激引起的 LFP 振幅明显增强。在对照大鼠中，MT 上的θ爆发刺激可靠地诱导了 ACC 中的 LFP 长时程增强，但在 14 天 EOI 大鼠中被阻断。将 AMPA/kainate 受体拮抗剂 CNQX 微透析至 ACC 可减弱对照和 EOI 大鼠 MT 刺激引起的 ACC 中的 LFP。NMDA 受体亚单位 NR2B 拮抗剂 Ro 25-6981 给药至 ACC 可显著减轻 EOI 大鼠 MT 刺激引起的 LFP 增强，而不影响对照大鼠。Ro 25-6981 微透析至 ACC 可剂量依赖性地减轻 EOI 诱导的大鼠双侧咬肌疼痛。这些发现为急性咬合干扰持续时间延长增强 ACC 中的突触传递，进而介导慢性咀嚼肌疼痛提供了直接证据。
