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首页> 外文期刊>Journal of Neurophysiology >Sympathetic modulation of activity in Adelta- and C-primary nociceptive afferents after intradermal injection of capsaicin in rats.
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Sympathetic modulation of activity in Adelta- and C-primary nociceptive afferents after intradermal injection of capsaicin in rats.

机译：大鼠皮内注射辣椒素后，对Adelta-和C-主要伤害感受性传入细胞活性的交感调节。

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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.
机译：交感神经系统可调节神经性和炎性疼痛。在某些疼痛模型中，交感神经节后传出与周围伤害性传递的调节有关。这项研究的目的是检查皮内注射辣椒素（CAP）诱导的Adelta和C原发性传入伤害感受器的敏化作用，以了解交感冒传出的存在是否对敏化至关重要。在通过麻醉大鼠的传导速度确定了纤维类型之后，记录了胫神经的一次初级传入放电。在注射CAP（1％，15 mul）后，在经假性交感切除的大鼠中，一些Adelta和大多数C初级传入纤维对机械刺激的反应增强，但在注射后，Adelta和C纤维的增强反应均降低了。交感神经节后传出。去甲肾上腺素通过动脉内注射进行外周预处理可以在交感神经切除条件下恢复并延长CAP诱导的反应增强。在交感完整的大鼠中，用α（1）-肾上腺素能受体拮抗剂（特拉唑嗪）进行的预处理在交感完整的大鼠中CAP注射后完全阻断了C纤维的增强反应，而没有显着影响Adelta纤维的增强反应。相比之下，育亨宾对α（2）-肾上腺素受体的阻断仅稍微降低了CAP诱发的反应增强。我们得出结论，交感神经传出的存在对于CAP诱导的Adelta和C初级传入纤维对机械刺激的致敏作用至关重要，并且α（1）-肾上腺素受体在C感受态敏感性的交感神经调节中起主要作用在外围。

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