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The enteric nervous system (ENS) sensory nerve endings in the colonic mucosa are specialized terminals that detect mechanical and chemical stimuli within the gut lumen (Furness, 2006). These endings belong to both intrinsic primary afferent neurons (IPANs), which reside entirely within the gut wall, and extrinsic primary afferent neurons, which transmit signals to the central nervous system via vagal or spinal pathways (Grundy & Schemann, 2007). They play a pivotal role in regulating gastrointestinal motility, secretion, and blood flow by initiating local reflex arcs and conveying sensory information such as pain and satiety (Bulmer & Knowles, 2013). In pathological states like irritable bowel syndrome (IBS), these nerve endings often exhibit hypersensitivity, contributing to chronic abdominal pain and altered bowel habits (Black & Ford, 2020). Therapeutic strategies frequently target molecular receptors expressed on these terminals, including 5-HT3, 5-HT4, and TRPV1 receptors, to modulate sensory input and alleviate symptoms (Gershon, 2013). For instance, linaclotide reduces visceral pain by decreasing the activity of colonic sensory neurons through a cGMP-mediated mechanism (Castro et al., 2013).
Modulation of neurotransmitter receptors (e.g., 5-HT3, 5-HT4) or ion channels (e.g., TRPV1, Nav1.7) located on sensory terminals to alter afferent signaling to the CNS or local enteric circuits.
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