scispace - formally typeset
G

Gary M. Mawe

Researcher at University of Vermont

Publications -  174
Citations -  9403

Gary M. Mawe is an academic researcher from University of Vermont. The author has contributed to research in topics: Enteric nervous system & Myenteric plexus. The author has an hindex of 48, co-authored 163 publications receiving 8446 citations. Previous affiliations of Gary M. Mawe include University of Calgary.

Papers
More filters
Journal ArticleDOI

Serotonin signalling in the gut—functions, dysfunctions and therapeutic targets

TL;DR: Emerging evidence suggests that exploiting epithelial targets with nonabsorbable serotonergic agents could provide safe and effective therapies, and this work provides an overview of theseserotonergic actions and treatment strategies.
Journal ArticleDOI

Molecular defects in mucosal serotonin content and decreased serotonin reuptake transporter in ulcerative colitis and irritable bowel syndrome

TL;DR: Findings support the assertion that disordered gastrointestinal function in IBS involves changes intrinsic to the bowel and suggest that shared defects in 5-HT signaling may underlie the altered motility, secretion, and sensation.
Journal ArticleDOI

Activation of neuronal P2X7 receptor-pannexin-1 mediates death of enteric neurons during colitis.

TL;DR: It is reported that inflammation causes enteric neuron death by activating a neuronal signaling complex composed of P2X7 receptors, pannexin-1 channels, the Asc adaptor protein and caspases, and it is concluded that activation of neuronal Panx1 underlies neuron death and the subsequent development of abnormal gut motility in IBD.
Journal ArticleDOI

Fundamentals of neurogastroenterology: Basic science

TL;DR: This review examines the fundamentals of neurogastroenterology that may underlie the pathophysiology of functional GI disorders (FGIDs) and emphasizes recent advances in understanding of the enteric nervous system, sensory physiology underlying pain, and stress signaling pathways.
Journal ArticleDOI

Serotonin availability is increased in mucosa of guinea pigs with TNBS-induced colitis.

TL;DR: Altered 5-HT availability may contribute to the dysmotility of inflammatory bowel disease, possibly due to desensitization of 5- HT receptors.