A unifying purinergic hypothesis for the initiation of pain.
There have been hints over the years about the involvement of purines in pain, and we now have direct evidence with the cloning and characterisation of extracellular receptors for ATP (P2X-purinoceptors) on nociceptive sensory neurons. In this article, a hypothesis is put forward about the sources of ATP released to activate these receptors in three different pain conditions--as a cotransmitter from sympathetic nerves in causalgia and reflex sympathetic dystrophy; from endothelial cells in vascular pain, including migraine and angina; and from tumour cells in cancer. These findings are leading to an active search for selective P2-purinoceptor antagonists to alleviate pain.
Burnstock
G
G
Department of Anatomy and Developmental Biology, University College London, UK.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D002422:Causalgia / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D009369:Neoplasms / Q000503:physiopathology; D009475:Neurons, Afferent / Q000502:physiology; D010146:Pain / Q000503:physiopathology*; D018048:Receptors, Purinergic P2 / Q000502:physiology*; D012019:Reflex Sympathetic Dystrophy / Q000503:physiopathology; D014652:Vascular Diseases / Q000503:physiopathology
D018048:Receptors, Purinergic P2; D000255:Adenosine Triphosphate