Tariba Knežević Petra, Vukman Robert, Antonić Robert, Kovač Zoran, Uhač Ivone, Simonić-Kocijan Sunčana
Petra Tariba Knežević, Department of Prosthodontics, University of Rijeka School of Dental Medicine and School of Medicine, Kreąimirova 40, 51000 Rijeka, Croatia,
Croat Med J. 2016 Dec 31;57(6):530-539. doi: 10.3325/cmj.2016.57.530.
To determine the relationship between bilateral allodynia induced by masseter inflammation and P2X3 receptor expression changes in trigeminal ganglia (TRG) and the influence of intramasseteric P2X3 antagonist administration on bilateral masseter allodynia.
To induce bilateral allodynia, rats received a unilateral injection of complete Freund's adjuvant (CFA) into the masseter muscle. Bilateral head withdrawal threshold (HWT) was measured 4 days later. Behavioral measurements were followed by bilateral masseter muscle and TRG dissection. Masseter tissue was evaluated histopathologically and TRG tissue was analyzed for P2X3 receptor mRNA expression by using quantitative real-time polymerase chain reaction (PCR) analysis. To assess the P2X3 receptor involvement in nocifensive behavior, two doses (6 and 60 μg/50 μL) of selective P2X3 antagonist A-317491 were administrated into the inflamed masseter muscle 4 days after the CFA injection. Bilateral HWT was measured at 15-, 30-, 60-, and 120-minute time points.
HWT was bilaterally reduced after the CFA injection (P<0.001). Intramasseteric inflammation was confirmed ipsilaterally to the CFA injection. Quantitative real-time PCR analysis demonstrated enhanced P2X3 expression in TRG ipsilaterally to CFA administration (P<0.01). In comparison with controls, the dose of 6 μg of A-317491 significantly increased bilateral HWT at 15-, 30-, and 60-minute time points after the A-317491 administration (P<0.001), whereas the dose of 60 μg of A-317491 was efficient at all time points ipsilaterally (P=0.004) and at 15-, 30-, and 60-minute time points contralaterally (P<0.001).
Unilateral masseter inflammation can induce bilateral allodynia in rats. The study provided evidence that P2X3 receptors can functionally influence masseter muscle allodynia and suggested that P2X3 receptors expressed in TRG neurons are involved in masseter inflammatory pain conditions.
确定咬肌炎症诱导的双侧痛觉过敏与三叉神经节（TRG）中P2X3受体表达变化之间的关系，以及咬肌内注射P2X3拮抗剂对双侧咬肌痛觉过敏的影响。
为诱导双侧痛觉过敏，给大鼠单侧咬肌注射完全弗氏佐剂（CFA）。4天后测量双侧头部撤离阈值（HWT）。行为测量后进行双侧咬肌和TRG解剖。对咬肌组织进行组织病理学评估，并用定量实时聚合酶链反应（PCR）分析TRG组织中P2X3受体mRNA表达。为评估P2X3受体在伤害性防御行为中的作用，在注射CFA 4天后，将两剂量（6和60μg/50μL）的选择性P2X3拮抗剂A-317491注射到发炎的咬肌中。在15、30、60和120分钟时间点测量双侧HWT。
注射CFA后双侧HWT降低（P<0.001）。在CFA注射侧同侧证实有咬肌内炎症。定量实时PCR分析表明，在给予CFA同侧的TRG中P2X3表达增强（P<0.01）。与对照组相比，6μg A-317491剂量在给予A-317491后15、30和60分钟时间点显著增加双侧HWT（P<0.001），而60μg A-317491剂量在同侧所有时间点均有效（P=0.004），在对侧15、30和60分钟时间点也有效（P<0.001）。
单侧咬肌炎症可诱导大鼠双侧痛觉过敏。该研究提供了证据表明P2X3受体可在功能上影响咬肌痛觉过敏，并提示TRG神经元中表达的P2X3受体参与咬肌炎性疼痛状态。
