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Capsaicin cream for neuropathic pain9/4/2023 More recent findings in the mouse indicate that pharmacological ablation of the central branches of TRPV1 nociceptors with capsaicin results in a more complete loss of acute sensitivity to heat pain than that observed in knockout constructs (table 1). It has been known for some time that intrathecal administration of capsaicin in rats causes long-lasting loss of heat sensitivity and can induce selective degeneration of a distinct population of primary sensory neurons involved in the mediation of chemogenic pain. Whereas TRPV1 knockout animals lack a component of sensory transduction in an otherwise intact neuronal circuit, intrathecal injection of capsaicin breaks the connection that all capsaicin-sensitive fibers have with the spinal cord. However, responsiveness to noxious heat stimuli is not completely lost in TRPV1 knockout mice. Rodents lacking the TRPV1 channel are not only insensitive to vanilloid-evoked acute pain, but also exhibit impairment in their ability to detect thermal stimuli and to develop thermal hyperalgesia (table 1). Several molecular biology and pharmacological techniques have been employed to elucidate the role of the TRPV1 receptor in somatosensory pathways. Data from clinical practice will determine if the high-concentration capsaicin patch is effective in real-world settings. In three recent randomized controlled trials, a patch containing high-concentration capsaicin demonstrated meaningful efficacy and tolerability relative to a low-concentration capsaicin control patch in patients with peripheral neuropathic pain. Topical application of capsaicin at the peripheral terminal of TRPV1-expressing neurons superficially denervates the epidermis in humans in a highly selective manner and results in hypoalgesia. Knockout studies have revealed the importance of TRPV1 as a molecular pain integrator and target for novel analgesic agents. Capsaicin is a highly selective agonist for the transient receptor potential channel vanilloid-receptor type 1 (TRPV1), which is expressed on central and peripheral terminals of nociceptive primary sensory neurons. This review article documents the clinical development of capsaicin to demonstrate that pharmacognosy still has a profound influence on modern-day drug development programs. Capsaicin has long been used as a traditional medicine to treat pain and, recently, its mechanism of analgesic action has been discovered.
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