ACC Plasticity Maintains Masseter Hyperalgesia Caused by Occlusal Interference
ACC Plasticity Maintains Masseter Hyperalgesia Caused by Occlusal Interference
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ACC 可塑性维持咬合干扰引起的咬肌痛觉过敏
DOI：
10.1177/0022034519827590
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发表时间：
2019-05-01
影响因子：
7.6
通讯作者：
Xie, Q. F.
中科院分区：
文献类型：
--
作者：
Xu, X. X.;Cao, Y.;Xie, Q. F.
在牙科治疗中，不适当的咬合改变会引起急性咬合干扰，从而导致慢性咀嚼肌疼痛。根本机制尚未阐明。前扣带皮层（ACC）的突触可塑性在慢性疼痛状态中起着关键作用。本研究旨在探讨前扣带回突触可塑性在急性咬合干扰引起的慢性咀嚼肌痛中的作用。建立大鼠实验性咬合干扰模型。采用在体局部场电位（LFP）记录方法，观察EOI作用后内侧丘脑（MT）至ACC的突触强度和可塑性的变化。检查了将谷氨酸受体拮抗剂微透析到ACC对从MT到ACC的突触传递的影响。此外，研究了抑制ACC中谷氨酸受体对EOI诱导的大鼠咬肌机械性痛觉过敏的影响。从EOI应用14 d开始，MT刺激引起的ACC LFP幅度显著增强。LFP在ACC的长时程增强是可靠地诱导theta爆发刺激MT在对照组大鼠，但闭塞在14天EOI大鼠。微透析入ACC的AMPA/红藻氨酸受体拮抗剂CNQX减弱了对照组和EOI大鼠由刺激MT引起的ACC中的LFP。ACC内注射NMDA受体NR 2B亚单位拮抗剂Ro 25-6981可显著减轻MT刺激诱发的EOI大鼠ACC LFP增强作用，而对对照组无明显影响。将Ro 25-6981微透析入ACC后，EOI诱导的大鼠双侧咬肌痛觉过敏呈剂量依赖性缓解。这些发现提供了直接证据，表明长时间的急性咬合干扰增强了ACC中的突触传递，进而介导了慢性咀嚼肌疼痛。
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.