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Annika B. Malmberg

    Turning up the heat on pain: TRPV1 receptors in pain and inflammation
    Mechanisms and mediators of neuropathic pain
    • Numerous improvements in our understanding of the mechanisms that underlie neuropathic pain states have come from the development of animal models, most of which involve partial peripheral nerve injury. The animal models have shown that nerve injury initiates a cascade of events resulting in altered neurochemistry and molecular biology of the peripheral neurons, the dorsal root ganglion cell, and changes in neurotransmitter and receptor expression in the dorsal horn of the spinal cord. Moreover, nerve injury produces anatomical changes with functional consequences. This volume summarises the current understanding of the pathophysiological processes in the peripheral and central nervous system that contribute to the neuropathic pain. It provides a timely review of neuropathic pain mechanisms, written by experts in the field.

      Mechanisms and mediators of neuropathic pain
    • Despite significant advancements in understanding the sensory nervous system, few innovative medicines for pain and inflammation have emerged. Many patients still rely on traditional analgesic and anti-inflammatory medications that originated from herbal remedies. New potential medicines based on capsaicin and its receptor draw from folk traditions while employing modern drug discovery techniques. The first formal documentation of capsaicin's pain-relieving properties dates back to 1850, although capsaicin-containing extracts had been used as folk medicines long before, similar to poppy or willow-bark extracts. It wasn't until 1878 that the selective action of capsaicin on the sensory nervous system was recognized. Chapter 1 features Janos Szolcsányi's review of early research, culminating in the pivotal studies by Nicholas Jansco and colleagues in the 1940s. Since then, capsaicin and related vanilloid compounds have been integral to investigations of analgesia and inflammation due to their ability to selectively activate a subset of sensory neurons, leading to sensations of pain and localized redness.

      Turning up the heat on pain: TRPV1 receptors in pain and inflammation