Myenteric plexus (Auerbach plexus) (None established for the myenteric plexus, though "ENS" is commonly used for the enteric nervous system)

The intestinal nerve plexus specifically refers to the interconnected networks of autonomic nerve fibers and ganglia regulating intestinal function—primarily the myenteric plexus (Auerbach plexus) and submucosal plexus (Meissner plexus). The myenteric plexus is situated between the muscle layers of the gut and is the main controller of gastrointestinal motility, coordinating peristaltic and segmental contractions through a combination of excitatory (cholinergic, tachykinin) and inhibitory (nitrergic, VIP) neurons. It contains a variety of neuron types: sensory (IPANs), interneurons, and motor neurons. Function and signaling are mediated by several neurotransmitters, with regulation from both the local environment and the central nervous system via the vagus nerve. Dysfunction of this plexus causes significant gastrointestinal disorders. While individual molecular targets (e.g., neurotransmitter receptors, enzymes) found within the plexus are targeted therapeutically, the plexus itself is not considered a specific drug target but a tissue system encompassing many such targets[1][2][3][4][7]. For therapeutic targeting or structured annotation, precise molecular entities or receptors within the plexus should be named (e.g., "muscarinic acetylcholine receptor M3," "neuronal nitric oxide synthase") rather than the general network ("intestinal nerve plexus"), which is an anatomical term, not a canonical molecular target[1][2][3].

Other names

Myenteric plexus (Auerbach plexus)Submucosal plexus (Meissner plexus)Enteric nervous system (ENS) (umbrella term for both plexuses)Digestive nerve plexusIntestinal nerve plexus (non-specific, not commonly used in modern research)

Drugs target specific neurotransmitter receptors, ion channels, or enzymes within ENS neurons to modulate motility and/or secretion—e.g., stimulation or blockade of muscarinic, serotonergic, or nitrergic signaling alters peristalsis and smooth muscle activity