Prospects & Overviews
Purinergic signalling: Its unpopular beginning, its acceptance and its exciting future
Version of Record online: 11 JAN 2012
Copyright © 2012 WILEY Periodicals, Inc.
Volume 34, Issue 3, pages 218–225, March 2012
How to Cite
Burnstock, G. (2012), Purinergic signalling: Its unpopular beginning, its acceptance and its exciting future. Bioessays, 34: 218–225. doi: 10.1002/bies.201100130
- Issue online: 13 FEB 2012
- Version of Record online: 11 JAN 2012
- ATP release and breakdown;
- neurodegenerative diseases;
- purinergic neuropathology;
Adenosine 5′-triphosphate (ATP) was identified in 1970 as the transmitter responsible for non-adrenergic, non-cholinergic neurotransmission in the gut and bladder and the term ‘purinergic’ was coined. Purinergic cotransmission was proposed in 1976 and ATP is now recognized as a cotransmitter in all nerves in the peripheral and central nervous systems. P1 (adenosine) and P2 (ATP) receptors were distinguished in 1978. Cloning of these receptors in the early 1990s was a turning point in the acceptance of the purinergic signalling hypothesis. There are both short-term purinergic signalling in neurotransmission, neuromodulation and secretion and long-term (trophic) purinergic signalling of cell proliferation, differentiation and death in development and regeneration. Much is known about the mechanisms of ATP release and its breakdown by ectonucleotidases. Recently, there has been emphasis on purinergic pathophysiology, including neurodegenerative and neuropsychiatric disorders. Purinergic therapeutic strategies are being developed for treatment of gut, kidney, bladder, lung, skeletal and reproductive system disorders, pain and cancer.