皮肤炎症改变豚鼠的痛觉感受器电生理,而大鼠没有。

0 MEDICINE, RESEARCH & EXPERIMENTAL
Laiche Djouhri, Ahmed Eliwa, Alghalya Al-Emadi, Yehia Y Hussein, Hissa Al-Suwaidi, Al-Jouhara Albaloshi, Ayman Mustafa, Mohammed Seed Ahmed
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引用次数: 0

摘要

炎性疼痛超敏反应被认为部分是由伤害性背根神经节(DRG)神经元兴奋性增加引起的。我们之前在豚鼠身上证明,后肢炎症会引起这些神经元的电生理变化,包括更快的动作电位(AP)和后超极化(AHP)动力学。考虑到大鼠和豚鼠是不同的物种,在遗传组成和生理上存在显著差异,我们假设皮肤炎症会对大鼠(疼痛研究的主要啮齿动物模型)的伤害性DRG神经元的电生理特性产生不同的影响。为了验证这一假设,我们对深度麻醉、未治疗(对照组)和完全弗氏佐剂(CFA)治疗的大鼠和豚鼠进行了DRG神经元(n = 430)的细胞内电压记录。C-、Aδ-和a β-痛觉感受器根据它们的背根传导速度(CVs)和对自然有害刺激的反应来鉴定。与我们的假设一致,我们观察到,在cfa诱导的后肢炎症发生4天后,大鼠伤害神经元的任何电生理变量都没有显著变化。相比之下,豚鼠伤害感受器表现出CV显著增加,AP和AHP持续时间显著减少。炎症引起的绝对不应期和相对不应期的缩短可能导致痛觉神经纤维的放电频率增加,从而促进炎症性疼痛超敏反应。这些发现表明,大鼠和豚鼠之间DRG神经元中离子通道表达和/或功能的差异可能导致炎症性疼痛的周围神经元机制存在物种特异性差异。鉴于豚鼠和人类在遗传和代谢方面的相似性,需要进一步的研究来确定豚鼠是否可以作为比大鼠更准确的慢性炎症性疼痛模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cutaneous inflammation alters nociceptor electrophysiology in guinea pigs but not rats.

Inflammatory pain hypersensitivity is believed to result, in part, from increased excitability of nociceptive dorsal root ganglion (DRG) neurons. We previously demonstrated in guinea pigs that hindlimb inflammation induces electrophysiological changes in these neurons, including faster action potential (AP) and afterhyperpolarization (AHP) kinetics. Given that rats and guinea pigs are distinct species with notable differences in genetic composition and physiology, we hypothesized that cutaneous inflammation would have different effects on the electrophysiological properties of nociceptive DRG neurons in rats-the predominant rodent model for pain research. To test this hypothesis, we performed intracellular voltage recordings from DRG neurons (n = 430) in deeply anesthetized, untreated (control) and complete Freund's adjuvant (CFA)-treated rats and guinea pigs. C-, Aδ-, and Aβ-nociceptors were identified based on their dorsal root conduction velocities (CVs) and responses to natural noxious stimuli. Consistent with our hypothesis, we observed no significant changes in any electrophysiological variables in rat nociceptive neurons four days after CFA-induced hindlimb inflammation. In contrast, guinea pig nociceptors exhibited a significant increase in CV and significant decreases in both AP and AHP durations. The inflammation-induced shortening of absolute and relative refractory periods likely contributes to increased firing frequency in nociceptive nerve fibers, thereby promoting inflammatory pain hypersensitivity. These findings suggest species-specific differences in peripheral neuronal mechanisms underlying inflammatory pain, potentially due to variation in ion channel expression and/or function in DRG neurons between rats and guinea pigs. Given the genetic and metabolic similarities between guinea pigs and humans, further research is warranted to determine whether guinea pigs may serve as a more accurate model of chronic inflammatory pain than rats.

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