Sympathetic modulation of activity in Adelta- and C-primary nociceptive afferents after intradermal injection of capsaicin in rats.
Sympathetic modulation of activity in Adelta- and C-primary nociceptive afferents after intradermal injection of capsaicin in rats.
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DOI：
10.1152/jn.00804.2004
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发表时间：
2005
影响因子：
2.5
通讯作者：
Yong Ren;X. Zou;L. Fang;Q. Lin
中科院分区：
文献类型：
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作者：
Yong Ren;X. Zou;L. Fang;Q. Lin
神经性和炎症性疼痛可由交感神经系统调节。在一些疼痛模型中，交感神经节后传出神经参与了外周伤害性传递的调节。本研究的目的是研究皮内注射辣椒素（capsaicin， CAP）对Adelta-和c -初级传入伤害感受器的致敏作用，以了解交感传入的存在是否对致敏作用至关重要。麻醉大鼠经传导速度鉴定纤维类型后，记录胫骨神经单次传入放电。在假交感神经切除大鼠中，注射CAP （1%, 15 μ l）后，一些Adelta-和大多数c -初级传入纤维对机械刺激的反应增强，但在去除交感神经节后传入神经后，Adelta-和c -纤维的增强反应减弱。动脉内注射去甲肾上腺素外周预处理可恢复和延长交感神经状态下cap诱导的反应增强。在交感完整大鼠中，α(1)-肾上腺素能受体拮抗剂（terazosin）预处理完全阻断了交感完整大鼠注射CAP后c -纤维的增强反应，而对adelta纤维的增强反应没有明显影响。相比之下，育亨宾对α(2)-肾上腺素能受体的阻断仅略微降低了cap引起的反应增强。我们得出结论，交感神经传出的存在对于cap诱导的Adelta-和C-primary传入纤维对机械刺激的敏化至关重要，α(1)-肾上腺素能受体在外周c -伤害感受器的交感调节中起主要作用。
Neuropathic and inflammatory pain can be modulated by the sympathetic nervous system. In some pain models, sympathetic postganglionic efferents are involved in the modulation of nociceptive transmission in the periphery. The purpose of this study is to examine the sensitization of Adelta- and C-primary afferent nociceptors induced by intradermal injection of capsaicin (CAP) to see whether the presence of sympathetic efferents is essential for the sensitization. Single primary afferent discharges were recorded from the tibial nerve after the fiber types were identified by conduction velocity in anesthetized rats. An enhanced response of some Adelta- and most C-primary afferent fibers to mechanical stimuli was seen in sham-sympathectomized rats after CAP (1%, 15 mul) injection, but the enhanced responses of both Adelta- and C-fibers were reduced after sympathetic postganglionic efferents were removed. Peripheral pretreatment with norepinephrine by intraarterial injection could restore and prolong the CAP-induced enhancement of responses under sympathectomized conditions. In sympathetically intact rats, pretreatment with an alpha(1)-adrenergic receptor antagonist (terazosin) blocked completely the enhanced responses of C-fibers after CAP injection in sympathetically intact rats without significantly affecting the enhanced responses of Adelta-fibers. In contrast, a blockade of alpha(2)-adrenergic receptors by yohimbine only slightly reduced the CAP-evoked enhancement of responses. We conclude that the presence of sympathetic efferents is essential for the CAP-induced sensitization of Adelta- and C-primary afferent fibers to mechanical stimuli and that alpha(1)-adrenergic receptors play a major role in the sympathetic modulation of C-nociceptor sensitivity in the periphery.