The myenteric plexus comprises various types of neurons, including excitatory and inhibitory motor neurons (referred to as parasympathetic postganglionic neurons), interneurons, and primary afferent neurons. Afferent neurons supply mechanoreceptors located within the gastrointestinal tract wall, forming the afferent limb of reflex arcs within the enteric plexus. Reflexes involving these mechanoreceptors are facilitated by local excitatory and inhibitory interneurons, which transmit signals through motor neurons to smooth muscle cells. Excitatory motor neurons release acetylcholine and substance P, while inhibitory motor neurons release dynorphin and vasoactive intestinal polypeptide. The enteric plexus possesses an extensive circuitry that allows it to coordinate the movements of a completely removed intestine. However, optimal function necessitates innervation by autonomic preganglionic neurons and regulation by the central nervous system.

The activity in the enteric nervous system is influenced by the sympathetic nervous system. Norepinephrine-containing sympathetic postganglionic neurons inhibit intestinal motility, those containing norepinephrine and neuropeptide Y regulate blood flow, and those containing norepinephrine and somatostatin control intestinal secretion. Intestinofugal neurons projecting back from the myenteric plexus to the sympathetic ganglia provide feedback.

The submucosal plexus plays a role in regulating ion and water transport across the intestinal epithelium, as well as glandular secretion. It communicates with the myenteric plexus to ensure coordination between the two components of the enteric nervous system. While the neurons and neural circuits of the submucosal plexus are less understood than those of the myenteric plexus, many neurons contain neuropeptides, and the neural networks are well organized.

The primary type of neuron found in autonomic ganglia is the postganglionic neuron, which receives synaptic connections from preganglionic neurons and projects to autonomic effector cells. Interneurons are also present in many autonomic ganglia, processing information within these ganglia. The enteric plexus can be considered as an intricate example of this type of processing. Some autonomic ganglia contain a type of interneuron called small, intensely fluorescent (SIF) cells, which have a high concentration of catecholamines and are believed to be inhibitory.

Acetylcholine serves as the classic neurotransmitter of autonomic ganglia, whether sympathetic or parasympathetic. The two classes of acetylcholine receptors in autonomic ganglia are nicotinic and muscarinic receptors, named after their responses to nicotine and muscarine alkaloids. Nicotinic receptors can be blocked by agents like curare or hexamethonium, while muscarinic receptors can be blocked by atropine. Nicotinic receptors in autonomic ganglia differ somewhat from those on skeletal muscle cells.

Both nicotinic and muscarinic receptors mediate excitatory postsynaptic potentials (EPSPs), but these potentials exhibit different time courses. Stimulation of preganglionic neurons elicits a rapid EPSP, followed by a slow EPSP. The fast EPSP is a result of nicotinic receptor activation, which opens ion channels. The slow EPSP is mediated by muscarinic receptors (primarily the M2 receptor), which inhibit the M current produced by potassium conductance.

Neurons in autonomic ganglia also release neuropeptides that act as neuromodulators. Apart from acetylcholine, sympathetic preganglionic neurons may release enkephalin, substance P, luteinizing hormone–releasing hormone, neurotensin, or somatostatin. Catecholamines such as norepinephrine and dopamine serve as neurotransmitters of SIF cells in autonomic ganglia.
The types of neurons found in the myenteric plexus include not only excitatory and inhibitory motor neurons (which can be considered parasympathetic postganglionic neurons) but also interneurons and primary afferent neurons. Afferent neurons supply mechanoreceptors within the wall of the gastrointestinal tract. These mechanoreceptors are the beginning of the afferent limb of reflex arcs within the enteric plexus. Local excitatory and inhibitory interneurons participate in these reflexes, and the output is sent through the motor neurons to smooth muscle cells. Excitatory motor neurons release acetylcholine and substance P; inhibitory motor neurons release dynorphin and vasoactive intestinal polypeptide. The circuitry of the enteric plexus is so extensive that it can coordinate the movements of an intestine that has been completely removed from the body. However, normal function requires innervation by the autonomic preganglionic neurons and regulation by the CNS.
Activity in the enteric nervous system is modulated by the sympathetic nervous system. Sympathetic post-ganglionic neurons that contain norepinephrine inhibit intestinal motility, those that contain norepinephrine and neuropeptide Y regulate blood flow, and those that contain norepinephrine and somatostatin control intestinal secretion. Feedback is provided by intestinofugal neurons that project back from the myenteric plexus to the sympathetic ganglia.
The submucosal plexus regulates ion and water transport across the intestinal epithelium and glandular secretion. It also communicates with the myenteric plexus to ensure coordination of the functions of the two components of the enteric nervous system. The neurons and neural circuits of the submucosal plexus are not as well understood as those of the myenteric plexus, but many of the neurons contain neuropeptides, and the neural networks are well organized.
The main type of neuron in autonomic ganglia is the post-ganglionic neuron. These cells receive synaptic connections from preganglionic neurons, and they project to autonomic effector cells. However, many autonomic ganglia also contain interneurons. These interneurons process information within the autonomic ganglia; the enteric plexus can be regarded as an elaborate example of this kind of processing. One type of interneuron found in some autonomic ganglia contains a high concentration of catecholamines; hence, these interneurons have been called small, intensely fluorescent (SIF) cells. SIF cells are believed to be inhibitory.
The classic neurotransmitter of autonomic ganglia, whether sympathetic or parasympathetic, is acetylcholine. The two classes of acetylcholine receptors in autonomic ganglia are nicotinic and muscarinic receptors, so named because of their responses to the plant alkaloids nicotine and muscarine. Nicotinic acetylcholine receptors can be blocked by such agents as curare or hexamethonium, and muscarinic receptors can be blocked by atropine. Nicotinic receptors in autonomic ganglia differ somewhat from those on skeletal muscle cells.
Nicotinic and muscarinic receptors both mediate excitatory postsynaptic potentials (EPSPs), but these potentials have different time courses. Stimulation of preganglionic neurons elicits a fast EPSP, followed by a slow EPSP. The fast EPSP results from activation of nicotinic receptors, which cause ion channels to open. The slow EPSP is mediated by muscarinic receptors (primarily the M2 receptor; see ) that inhibit the M current, a current produced by potassium conductance.
Neurons in autonomic ganglia also release neuropeptides that act as neuromodulators. Besides acetylcholine, sympathetic preganglionic neurons may release enkephalin, substance P, luteinizing hormone–releasing hormone, neurotensin, or somatostatin.
Catecholamines such as norepinephrine and dopamine serve as the neurotransmitters of SIF cells in autonomic ganglia.