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交感神经节后神经元参与大鼠辣椒素诱导的继发性痛觉过敏。

Involvement of the sympathetic postganglionic neuron in capsaicin-induced secondary hyperalgesia in the rat.

作者信息

Kinnman E, Levine J D

机构信息

Department of Anatomy, University of California, San Francisco 94143, USA.

出版信息

Neuroscience. 1995 Mar;65(1):283-91. doi: 10.1016/0306-4522(94)00474-j.

DOI:10.1016/0306-4522(94)00474-j
PMID:7753402
Abstract

The involvement of the sympathetic postganglionic neuron in secondary hyperalgesia was evaluated using a model of secondary hyperalgesia induced by a small intradermal injection of capsaicin in the rat, a procedure known to produce mechanical hyperalgesia/allodynia in humans. Capsaicin injection into the glabrous skin of the hind paw led to increased sensitivity to mechanical stimulation with von Frey filaments at the injection site (i.e. primary hyperalgesia) as well as in an area of the hind paw remote from the site of injection (i.e. secondary hyperalgesia). Surgical removal of the sympathetic postganglionic neurons innervating the hind paw plantar skin before the capsaicin injection prevented secondary hyperalgesia. However, decentralization of the sympathetic postganglionic neurons subserving the hind paw did not effect secondary hyperalgesia. Phentolamine, an alpha-adrenergic receptor antagonist, as well as prazosin, an alpha 1-adrenergic receptor antagonist, given systemically, both blocked the development of secondary hyperalgesia. Yohimbine, an alpha 2-adrenergic receptor antagonist, was without effect. Prazosin also blocked the development of secondary hyperalgesia when given intradermally at the site of capsaicin injection. Activation of C-fibres with capsaicin induces secondary hyperalgesia, which is sympathetic postganglionic neuron-dependent. This sensory-sympathetic interaction is, however, independent of preganglionic sympathetic outflow and seems to be mediated by an alpha 1-adrenergic mechanism. Sensory-sympathetic interaction appears to take place in the area of capsaicin-induced C-fibre nociceptor activation.

摘要

使用大鼠皮内小剂量注射辣椒素诱导继发性痛觉过敏的模型,评估交感神经节后神经元在继发性痛觉过敏中的作用,该方法在人类中可引发机械性痛觉过敏/异常性疼痛。将辣椒素注射到后爪无毛皮肤中,导致注射部位对von Frey细丝机械刺激的敏感性增加(即原发性痛觉过敏),以及后爪远离注射部位的区域(即继发性痛觉过敏)。在注射辣椒素之前,手术切除支配后爪足底皮肤的交感神经节后神经元可预防继发性痛觉过敏。然而,支配后爪的交感神经节后神经元去传入并不影响继发性痛觉过敏。全身性给予α-肾上腺素能受体拮抗剂酚妥拉明以及α1-肾上腺素能受体拮抗剂哌唑嗪,均可阻断继发性痛觉过敏的发展。α2-肾上腺素能受体拮抗剂育亨宾则无作用。在辣椒素注射部位皮内给予哌唑嗪也可阻断继发性痛觉过敏的发展。辣椒素激活C纤维可诱导继发性痛觉过敏,这依赖于交感神经节后神经元。然而,这种感觉-交感神经相互作用独立于节前交感神经传出,似乎由α1-肾上腺素能机制介导。感觉-交感神经相互作用似乎发生在辣椒素诱导的C纤维伤害性感受器激活区域。

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