Increased conduction velocity of nociceptive primary afferent neurons during unilateral hindlimb inflammation in the anaesthetised guinea-pig
Increased conduction velocity of nociceptive primary afferent neurons during unilateral hindlimb inflammation in the anaesthetised guinea-pig
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DOI：
10.1016/s0306-4522(00)00503-0
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发表时间：
2001-01-01
期刊：
影响因子：
3.3
通讯作者：
Lawson, SN
中科院分区：
文献类型：
--
作者：
Djouhri, L;Lawson, SN
在皮内注射完全弗氏佐剂至同侧腿部和足部诱导幼年豚鼠后肢炎症期间，伤害性背根神经节神经元胞体中的动作电位（C-和A-δ纤维单位）和后超极化（A-纤维单位）持续时间减少。在这里，我们提出的证据表明，这些伤害性神经元的单点传导速度（即在一个单一的传导距离估计）在这种类型的炎症增加。在两种类型的实验中，将麻醉的未处理豚鼠（对照）的单点传导速度与完全弗氏佐剂处理后2天和4天的单点传导速度进行比较。第一个涉及同侧L 6和S1背根神经节神经元胞体的细胞内电压记录。根据其背根传导速度将单位分类为C、A delta或A alpha/beta，并表征为伤害性。根据它们对机械和热刺激的反应，低阈值机械感受性或无反应。与未治疗的动物相比，完全弗氏佐剂治疗后4天，发现背根单点传导速度中位数的C纤维伤害性单位和A纤维伤害性单位分别显著增加54%和46%。这些增加在完全弗氏佐剂后4天比2天更大。治疗后4天，在低阈值机械感受器中也观察到相同方向的轻微趋势（10%），但不显著，但两天后就没有了。在治疗组和对照组动物中，用同侧S2背根和腓肠神经的复合动作电位记录证实了速度增加。记录显示C、A δ和A α/β波的单点速度增加的趋势，A δ波的上边界（即A δ和A α/β波之间的边界）在给药动物中的传导速度显著高于对照动物。这在S2背根和腓肠神经中均可见。在炎症过程中，引起背根神经和腓肠神经复合动作电位的C和A δ成分的平均电阈值也显著降低。未发现腓肠神经复合动作电位（C、A δ或A α/β）任何成分的利用时间减少的证据。传导速度的增加可能是由于某些离子通道类型的表达改变或激活/失活，例如Na+通道。本实验表明，后肢炎症引起了炎症期间伤害感受性初级传入神经元传导速度的显著增加，但低阈值机械感受性初级传入神经元的传导速度没有显著增加，以及：引起背根神经和腓肠神经复合动作电位的C和A δ成分的平均电阈值显著降低。这些变化，连同先前描述的炎症过程中伤害性神经元的动作电位形状的变化，可能反映了膜功能的改变，有助于炎症性痛觉过敏。(C)2001年IBRO。由Elsevier Science Ltd.出版，版权所有。
Decreases in durations of action potentials (C- and A delta -fibre units) and afterhyperpolarisations (A-fibre units) occur in somata of nociceptive dorsal root ganglion neurons during hindlimb inflammation induced in young guinea-pigs by intradermal injections of Complete Freund's Adjuvant into the ipsilateral leg and foot. Here we present evidence that the single-point conduction velocity (i.e. estimated over a single conduction distance) of these nociceptive neurons is increased during this type of inflammation. The single-point conduction velocities in anaesthetised untreated guinea-pigs (control) were compared with those two and four days after Complete Freund's Adjuvant treatment in two types of experiment. The first involved intracellular voltage recordings from somata of ipsilateral L6 and S1 dorsal root ganglion neurons. Units were classified as C, A delta or A alpha/beta on the basis of their dorsal root conduction velocities and characterised as nociceptive. low-threshold mechanoreceptive or unresponsive according to their responses to mechanical and thermal stimuli. Compared with untreated animals, significant increases of 54% for C-fibre nociceptive units and 46% for A-fibre nociceptive units in the medians of dorsal root single-point conduction velocities were found four days after Complete Freund's Adjuvant treatment. These increases were greater at four days than at two days after Complete Freund's Adjuvant. A slight tendency in the same direction (10%) that was not significant was also seen in low-threshold mechanoreceptors Four days after treatment, but not after two days. The increased velocities were confirmed with compound action potential recordings from ipsilateral S2 dorsal roots and sural nerves, in treated and control animals. Recordings showed a tendency for increased single-point velocities in C, A delta and A alpha/beta waves, with the upper border of the A delta wave (i.e. the border between A delta and A alpha/beta waves) falling at a significantly higher conduction velocity in treated than control animals. This was seen both in S2 dorsal roots and in sural nerves. There was also a significant decrease in the mean electrical threshold For eliciting the C and A delta components of compound action potentials of both dorsal root and sural nerves during inflammation. No evidence was found for a reduction in utilisation time for any components of the sural nerve compound action potential (C, A delta or A alpha/beta). The conduction velocity increases may be due to altered expression or activation/inactivation of certain ion channel types, such as Na+ channels.The present experiments demonstrate that, hindlimb inflammation caused a significant increase in conduction velocity of nociceptive but not of low-threshold mechanoreceptive primary afferent neurons during inflammation, as well as: a significant decrease in the mean electrical threshold for eliciting the C and A delta components of compound action potentials of both dorsal root and sural nerves. These changes, together with the previously described changes in the action potential shape of nociceptive neurons during inflammation, probably reflect alterations in membrane function that contribute to inflammatory hyperalgesia. (C) 2001 IBRO. published by Elsevier Science Ltd. All rights reserved.