Abstract
Intraplantar (i.pl.) injection of small doses of capsaicin has been shown to produce hyperalgesia and upregulation of the levels of proinflammatory cytokines. The present work aimed at investigating the possible mediation of these effects by sensory neuropeptides and mast cells. Various groups of rats received i.pl. injection of capsaicin alone or preceded by the injection of antagonists to substance P (SP), calcitonin gene-related protein (CGRP) and histamine (H1, H2) or the mast cell blocker ketotifen. All pretreatments prevented, in a dose-related manner, the capsaicin-induced hyperalgesia. The SP, H2 antagonists and ketotifen prevented the upregulation of all cytokines and nerve growth factor (NGF) levels, while the CGRP and H1 antagonists showed only attenuation of the NGF level.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Analgesics / pharmacology
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Animals
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Behavior, Animal
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Calcitonin Gene-Related Peptide / antagonists & inhibitors
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Calcitonin Gene-Related Peptide / physiology*
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Capsaicin / pharmacology*
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Cytokines / metabolism*
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Dose-Response Relationship, Drug
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Drug Interactions
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Histamine / physiology*
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Histamine Antagonists / pharmacology
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Hyperalgesia / chemically induced
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Hyperalgesia / metabolism*
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Injections, Spinal / methods
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Nerve Growth Factor / metabolism
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Pain Measurement / drug effects
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Rats
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Rats, Sprague-Dawley
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Reaction Time / drug effects
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Substance P / analogs & derivatives*
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Substance P / antagonists & inhibitors
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Substance P / pharmacology
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Substance P / physiology*
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Time Factors
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Up-Regulation / drug effects
Substances
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Analgesics
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Cytokines
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Histamine Antagonists
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spantide II
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Substance P
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Histamine
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Nerve Growth Factor
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Calcitonin Gene-Related Peptide
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Capsaicin