Expanding field of purinergic signaling

Burnstock, Geoffrey

doi:10.1002/ddr.1093

Cited by 39 publications

(19 citation statements)

References 127 publications

(105 reference statements)

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“…ATP released during extreme (colic) distension also acts on P2X 3 and/or P2X 2/3 receptors on high-threshold extrinsic sensory nerve fibres (labelled with isolectin B4 (IB 4 )) that send messages via the dorsal root ganglia (DRG) to pain centres in the central nervous system. (From [256], reproduced with permission from Wiley-Liss, Inc.). ute to touch evoked pain [125].…”

Section: Skinmentioning

confidence: 97%

Purinergic Receptors and Pain

Burnstock¹

2009

CPD

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178

146

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There is a brief summary of the early background literature about purinergic signalling and its involvement in pain, of ATP storage, release and ectoenzymatic breakdown and of the current classification of receptor subtypes for purines and pyrimidines. The review then focuses on purinergic mechanosensory transduction involved in visceral, cutaneous and musculoskeletal nociception and on the roles played by P2X-(3), P2Y(2/3), P2X(4), P2X(7) and P2Y(12) receptors in neuropathic and inflammatory pain. Current developments of compounds for the therapeutic treatment of both visceral and neuropathic pain are discussed.

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Section: Skinmentioning

confidence: 97%

Purinergic Receptors and Pain

Burnstock¹

2009

CPD

Self Cite

178

146

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“…The ATP released during extreme (colic) distension also acts on P2X3 and/or P2X2/3 receptors on high-threshold extrinsic sensory nerve fibres [labelled with isolectin B4 (IB 4 )] that send messages via the dorsal root ganglia (DRG) to pain centres in the CNS. [From Burnstock (2001), reproduced with permission from Wiley. ]…”

Section: Purinergic Pathophysiology and Therapeutic Potentialmentioning

confidence: 99%

“…It should be noted that the list of elements is not meant to be all-inclusive. & Burnstock, 2001;Lazarowski et al 2011;Lazarowski, 2012). Scientists involved are shown in Fig.…”

Section: Release Of Atp and Purinergic Mechanosensory Transductionmentioning

confidence: 99%

Purinergic signalling: from discovery to current developments

Burnstock

2014

Experimental Physiology

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204

207

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New FindingsWhat is the topic of this review?This is a personal historical review about the discovery and the main conceptual advances leading to our current understanding of purinergic signalling. The contributions of leading figures in the field are acknowledged. It includes the discovery of purinergic neuromuscular and synaptic transmission, cotransmission, the identification of P1 (adenosine), P2X nucleotide ion channel and P2Y nucleotide G protein-coupled receptors, the identity of ectonucleotidases and release of ATP from cells by mechanical stimulation and mechanosensory transduction.What advances does it highlight?It highlights the pathophysiology of purinergic signalling and recent therapeutic developments.This lecture is about the history of the purinergic signalling concept. It begins with reference to the paper by Paton & Vane published in 1963, which identified non-cholinergic relaxation in response to vagal nerve stimulation in several species, although they suggested that it might be due to sympathetic adrenergic nerves in the vagal nerve trunk. Using the sucrose gap technique for simultaneous mechanical and electrical recordings in smooth muscle (developed while in Feldberg’s department in the National Institute for Medical Research) of the guinea-pig taenia coli preparation (learned when working in Edith Bülbring’s smooth muscle laboratory in Oxford Pharmacology), we showed that the hyperpolarizations recorded in the presence of antagonists to the classical autonomic neurotransmitters, acetylcholine and noradrenaline, were inhibitory junction potentials in response to non-adrenergic, non-cholinergic neurotransmission, mediated by intrinsic enteric nerves controlled by vagal and sacral parasympathetic nerves. We then showed that ATP satisfied the criteria needed to identify a neurotransmitter released by these nerves. Subsequently, it was shown that ATP is a cotransmitter in all nerves in the peripheral and central nervous systems. The receptors for purines and pyrimidines were cloned and characterized in the early 1990s, and immunostaining showed that most non-neuronal cells as well as nerve cells expressed these receptors. The physiology and pathophysiology of purinergic signalling is discussed.

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“…(70) with permission from the American Physiological Society; and F reproduced from Ref. (80) with permission from Elsevier].…”

Section: Pathophysiology Of Purinergic Signalling In the Gutmentioning

confidence: 99%

The journey to establish purinergic signalling in the gut

Burnstock

2008

Neurogastroenterology Motil

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Gastroenteropathy causes considerable morbidity in patients with diabetes mellitus and represents a major healthcare burden. Current treatments are largely symptomatic and frequently ineffective. Development of new therapeutic options is hampered by poor understanding of the underlying pathomechanisms. Experimental studies and sparse human data indicate that diabetic gastroenteropathy is multifactorial and involves not only parasympathetic and sympathetic autonomic nerves, but also enteric neurons, smooth muscle cells and interstitial cells of Cajal (ICC). ICC are mesenchymal cells that occur throughout the muscular coat of the gastrointestinal tract and provide functions critical for normal gastrointestinal motility including generation and propagation of electrical slow waves and mediation of bidirectional communication between the autonomic nervous system and smooth muscle cells. Through these functions, and in concert with other cell types of the gastrointestinal muscles, ICC support basic gastrointestinal functions such as digestion, absorption and waste removal. Loss or dysfunction of ICC in various dysmotilities and their animal models has been shown to lead to gastric dysrhythmias, gastroparesis, slow intestinal transit, impaired neuroeffector mechanisms and altered visceral afferent signalling that are considered hallmarks of diabetic gastroenteropathy. These findings and an increasing body of evidence indicating disruptions of ICC networks in diabetes suggest that the loss of ICC in this disorder is probably of functional significance and could even be a major pathogenetic factor. Future research should focus on the identification of the molecular and cellular mechanisms underlying ICC loss in diabetes and the translation of the experimental findings into treatments.

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Expanding field of purinergic signaling

Cited by 39 publications

References 127 publications

Purinergic Receptors and Pain

Purinergic Receptors and Pain

Purinergic signalling: from discovery to current developments

The journey to establish purinergic signalling in the gut

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