Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162473 (Frey)
 2,599 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Involvement of the sympathetic postganglionic neuron in capsaicin-induced secondary hyperalgesia in the rat. 775 2

It has been demonstrated recently that in addition to its spinal analgesic actions, the alpha 2 adrenoreceptor agonist clonidine also has peripheral analgesic activity. Few data are available regarding the antinociceptive effects of spinal vs peripherally delivered clonidine in inflammatory pain. Thus we have studied spinal (intrathecal = i.t.) and peripheral (intra-articular = i.a.) administration of clonidine in the rat inflamed knee joint model. Thermal and mechanical antinociception was assessed in rats over 28 h using a modified Hargreaves box and von Frey hairs after induction of tonic persistent inflammatory pain by injection of a kaolin-carrageenan mixture into the right knee joint. Thirty minutes after injection of kaolin-carrageenan, clonidine was administered via an i.t. catheter or by i.a. injection into the right inflamed knee joint or by subcutaneous injection (s.c.) (highest effective intra-articular dose). The specific site of action was assessed using the alpha 2 antagonist yohimbine i.t., i.a. or s.c. Clonidine i.t. resulted in thermal and mechanical antinociception during ongoing inflammation, which was not enhanced by inflammation. In contrast, i.a. delivery of clonidine, which also produced a dose-dependent thermal and mechanical antinociceptive effect, revealed a leftward shift in the antinociceptive activity produced by ongoing inflammation. Yohimbine inhibited the antinociceptive action of clonidine at the site of delivery. We suggest that clonidine produces potent thermal and mechanical antinociception regardless of the route of administration. However, chronic inflammatory processing appears to enhance the antinociceptive efficacy of the peripheral alpha 2 agonist.
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PMID:Thermal and mechanical antinociceptive action of spinal vs peripherally administered clonidine in the rat inflamed knee joint model. 1065 15