Plasticity of enteric nerve functions in the inflamed and postinflamed gut.
Inflammation of the gut alters the properties of the intrinsic and extrinsic neurons that innervate it. While the mechanisms of neuroplasticity differ amongst the inflammatory models that have been used, amongst various regions of the gut, and between intrinsic vs extrinsic neurons, a number of consistent features have been observed. For example, intrinsic and extrinsic primary afferent neurons become hyperexcitable in response to inflammation, and interneuronal synaptic transmission is facilitated in the enteric circuitry. These changes contribute to alterations in gut function and sensation in the inflamed bowel as well as functional disorders, and these changes persist for weeks beyond the point at which detectable inflammation has subsided. Thus, gaining a more thorough understanding of the mechanisms responsible for inflammation-induced neuroplasticity, and strategies to reverse these changes are clinically relevant goals. The purpose of this review is to summarize our current knowledge regarding neurophysiological changes that occur during and following intestinal inflammation, and to identify and address gaps in our knowledge regarding the role of enteric neuroplasticity in inflammatory and functional gastrointestinal disorders.
Department of Anatomy and Neurobiology, The University of Vermont College of Medicine, Burlington, VT 05405, USA. gary.mawe@uvm.edu
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Mawe
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Strong
K A
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Sharkey
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D004195:Disease Models, Animal; D017615:Enteric Nervous System / Q000033:anatomy & histology / Q000502:physiology*; D041981:Gastrointestinal Tract / Q000033:anatomy & histology / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology*; D011984:Sensory Receptor Cells / Q000378:metabolism; D050916:TRPV Cation Channels / Q000378:metabolism
D050916:TRPV Cation Channels