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Pain channelopathies
Author(s) -
Cregg Roman,
Momin Aliakmal,
Rugiero Francois,
Wood John N.,
Zhao Jing
Publication year - 2010
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.187807
Subject(s) - neuroscience , ion channel , trpv1 , sodium channel , analgesic , population , familial hemiplegic migraine , medicine , neuropathic pain , potassium channel , chronic pain , transient receptor potential channel , pharmacology , biology , migraine , chemistry , anesthesia , receptor , sodium , environmental health , organic chemistry , aura , migraine with aura
Pain remains a major clinical challenge, severely afflicting around 6% of the population at any one time. Channelopathies that underlie monogenic human pain syndromes are of great clinical relevance, as cell surface ion channels are tractable drug targets. The recent discovery that loss‐of‐function mutations in the sodium channel Nav1.7 underlie a recessive pain‐free state in otherwise normal people is particularly significant. Deletion of channel‐encoding genes in mice has also provided insights into mammalian pain mechanisms. Ion channels expressed by immune system cells (e.g. P2X7) have been shown to play a pivotal role in changing pain thresholds, whilst channels involved in sensory transduction (e.g. TRPV1), the regulation of neuronal excitability (potassium channels), action potential propagation (sodium channels) and neurotransmitter release (calcium channels) have all been shown to be potentially selective analgesic drug targets in some animal pain models. Migraine and visceral pain have also been associated with voltage‐gated ion channel mutations. Insights into such channelopathies thus provide us with a number of potential targets to control pain.