Lysophosphatidic acid signaling is the definitive mechanism underlying neuropathic pain

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Chemical mediators stimulate their receptors on nociceptor endings of sensory neurons, activate various types of ion channels through intracellular signaling, and generate action potentials.16 Transient receptor potential cation channel subfamily V member 1 (TRPV1) and acid-sensing ion channels and their family channels also play key roles in pain transmission caused by physiological stimuli (eg, heat, cold, and acids) and are modified by receptor signaling of chemical mediators.16,18,36 These mechanisms are categorized by acute pain with inflammatory or nociceptive features, have an adaptive role in an intact pain system, and play a part in the bioalarm system. Neuropathic pain (NP), on the other hand, occurs when the body receives direct damage to the pain pathway, from peripheral neurons to the cortex, and is chronic, with pain lasting for long periods even after the original damage has been resolved. Neuropathic pain manifests as abnormal pain symptoms, such as hyperalgesia and allodynia, and shows less sensitivity to anti-inflammatory drugs or opioid analgesics, which effectively suppress acute pain. Therefore, NP is considered to represent maladaptive functioning of the pain system. Fibromyalgia (FM) is another type of intractable chronic pain, although its cause remains elusive.12,13,46,81 Basic research studies are important to gain a better understanding of chronic pain and to control it through innovations in mechanism-based medicine.

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