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Enteric neurons in the colonic mucosa primarily constitute the submucosal (Meissner's) plexus, a network of neurons and glia located within the submucosal layer of the intestinal wall [1]. These neurons are essential for the local control of mucosal functions, including the regulation of epithelial electrolyte and water secretion, mucus production, and local blood flow [2]. They receive sensory information from the intestinal lumen and coordinate reflex responses through the release of various neurotransmitters such as acetylcholine, vasoactive intestinal peptide (VIP), and substance P [3]. In conditions like irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD), these neurons exhibit structural and functional changes, contributing to symptoms like visceral hypersensitivity and altered motility [1, 4]. Therapeutic agents often target specific receptors on these neurons, such as serotonin (5-HT3, 5-HT4) or opioid receptors, or act indirectly via epithelial mediators like cGMP to modulate gut physiology and alleviate clinical symptoms [3, 5]. The neuro-immune crosstalk involving these neurons is also a key factor in maintaining mucosal homeostasis and responding to inflammatory triggers [2]. Understanding the specific molecular profiles of these neurons is crucial for developing targeted therapies that minimize systemic side effects [3].
Modulation of neurotransmitter release and neuronal excitability via G protein-coupled receptors or indirect epithelial-derived mediators to regulate gastrointestinal motility and mucosal secretion [1, 3, 5].
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