![]() Mechanical allodynia was assessed once every 5 min over a 50-min period by light stroking of the skin of the hind paws and tail of the mice, twice each, with a paintbrush. After IT injection, each mouse was placed in an individual 13 × 8.5 × 13 cm Plexiglas enclosure with wood chips on the floor and observed. PGE 2 (10 ng per mouse) or PGF 2α (1 μg per mouse) dissolved in sterile saline (5 μL) was injected slowly into the subarachnoid space of vehicle- or capsaicin-pretreated mice. Briefly, a 27-gauge stainless-steel needle (0.35-mm outer diameter) attached to a microsyringe was inserted between the L5 and L6 vertebrae. Studies of allodynia were performed as described previously (14). ![]() Each application was of approximately 30 mg of cream, which was gently rubbed into the skin for about 10 s. Vehicle cream contained 18% polyoxyethylated castor oil, 17% liquid paraffin, 5% white Vaseline, 4% 1-hexadecanol, 0.1% EDTA disodium salt, and 0.75% triethanolamine. Mice had vehicle or 0.025%, 0.05%, or 0.1% capsaicin cream applied once to the anterior and lateral skin of hind paws and tail 24 h before behavioral experiments. This study was conducted with the approval of the Animal Experimentation Committee of Kansai Medical University and in accordance with the guidelines of the ethics committee of the International Association for the Study of Pain (16). The animals were used only for a single experiment. The mice were divided into various groups ( n = 6 per group for allodynia and n = 10 per group for the tail-flick test). Four-week-old mice weighing 20 ± 2 g were used in this study. The animals were housed under conditions of a 12-h light-dark cycle, a constant temperature of 22☌ ± 2☌, and 60% ± 10% humidity. Male ddY mice were obtained from Japan SLC (Hamamatsu, Japan). In this study, we therefore investigated the effect of capsaicin cream on PGE 2- and PGF 2α-induced allodynia. However, the complex mechanism by which capsaicin cream causes analgesia remains incompletely understood. We demonstrated that the selective elimination of C fibers by neonatal capsaicin treatment resulted in the disappearance of allodynia induced by PGE 2, but not that by PGF 2α (14).Ĭapsaicin cream (15) and lidocaine patch 5% are the only topical drugs approved by the Food and Drug Administration for the treatment of postherpetic neuralgia, patients suffering from which had scarred areas with abnormal sensation of light touch (mechanical allodynia), pain, or thermal change (warm or cold allodynia). We previously reported that the intrathecal (IT) administration of PGE 2 and PGF 2α into mice induced touch-evoked pain (allodynia) the mice showed squeaking, biting, and scratching behaviors in response to tactile stimuli (13). ![]() Recent evidence indicates that PGs are critical for the processing of pain, not only by sensitizing peripheral terminals of primary afferent nociceptors (6,7), but also by augmenting the processing of pain information at the spinal level (10–12). Because aspirinlike drugs suppress inflammatory responses, including pain, by blocking the synthesis of PGs as well as other effects relevant to suppression of inflammation (6–9), it has been widely accepted that PGs are involved in inflammation. Prostaglandins (PGs) are a group of bioactive lipids working as local mediators in virtually all tissues and include D, E, F, and I types (5). ![]() In fact, topical capsaicin has been tried as an analgesic in a variety of neuropathic pain conditions, such as postherpetic neuralgia, painful diabetic neuropathy, osteoarthritis, the postsurgical pain syndrome, and Guillain-Barré syndrome (1,2). This desensitization is the rationale that has led to the use of capsaicin as a therapeutic drug for pain relief. Continued application of capsaicin at small doses to adult animals causes a localized desensitization of nociceptive afferents that can last for several days to weeks. Capsaicin is a neurotoxin that, when a large dosage (50 mg/kg) is administered subcutaneously to neonatal animals, destroys a large subpopulation of small-diameter, mainly unmyelinated, primary afferent C fibers and probably thin-myelinated Aδ fibers (4). When it is applied topically to the skin of animals and humans, capsaicin initially lowers the threshold for thermal, chemical, and mechanical nociception by direct activation of vanilloid receptor 1 (3) on free nerve endings of C fibers. Capsaicin is a pungent component of hot chili peppers and has the chemical name trans-8-methyl- N-vanillyl-6-nonenamide (1,2). ![]()
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