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The **enteric nervous system** is a complex network of neurons embedded in the wall of the gastrointestinal tract that autonomously regulates digestive functions. It controls **peristalsis**, which is the rhythmic contraction and relaxation pattern that propels food through the gut. Peristalsis is orchestrated by local reflex circuits within the ENS—primarily via two major plexuses (the myenteric and submucosal plexuses)—and involves both excitatory and inhibitory neurotransmitters such as acetylcholine, substance P, nitric oxide, vasoactive intestinal peptide (VIP), ATP, serotonin (5‑HT), dopamine, and others[3][4][8]. The ENS can function independently from central input but also integrates signals from sympathetic and parasympathetic branches. **Peristalsis stimulation via enteric nervous system** does not refer to a specific molecular target like a receptor or enzyme; rather it describes an entire physiological process regulated by many cell types and signaling molecules. Therefore it cannot be considered a canonical therapeutic target itself but rather an outcome modulated by targeting specific receptors or pathways within this neural network[1][3][5]. Therapeutically relevant targets for stimulating peristalsis include various receptors on enteric neurons—such as serotonin 5‑HT4 receptors targeted by prokinetic drugs like prucalopride—or cholinergic pathways modulated by acetylcholine agonists/antagonists. In summary: "Peristalsis stimulation via enteric nervous system" refers to an integrated physiological process governed by multiple molecular targets within the ENS; it is not itself a discrete molecule/receptor suitable for structured drug-target annotation[1][3][8].
Modulation of neurotransmitter signaling within the ENS to enhance or inhibit peristaltic reflexes and smooth muscle contraction[3][5]
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