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Submucosal plexus
Submucosal plexus
Submucosal plexus
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Submucosal plexus
The plexus of the submucosa from the rabbit. X 50.
Details
Identifiers
Latinplexus nervosus submucosus, plexus submucosus,
plexus Meissneri
MeSHD013368
TA98A14.3.03.042
TA26728
FMA63252
Anatomical terms of neuroanatomy
This article is one of a series on the
Gastrointestinal wall
General structure
Specific
Organs

The submucosal plexus (Meissner's plexus, plexus of the submucosa, plexus submucosus) lies in the submucosa of the intestinal wall. The nerves of this plexus are derived from the myenteric plexus which itself is derived from the plexuses of parasympathetic nerves around the superior mesenteric artery. Branches from the myenteric plexus perforate the circular muscle fibers to form the submucosal plexus. Ganglia from the plexus extend into the muscularis mucosae and also extend into the mucous membrane.

They contain Dogiel cells.[1] The nerve bundles of the submucosal plexus are finer than those of the myenteric plexus. Its function is to innervate cells in the epithelial layer and the smooth muscle of the muscularis mucosae.

14% of submucosal plexus neurons are sensory neurons – Dogiel type II, also known as enteric primary afferent neurons or intrinsic primary afferent neurons.[2]

History

[edit]

Meissners' plexus was described by German professor Georg Meissner.[3]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Submucosal plexus

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The submucosal plexus, also known as Meissner's plexus, is a network of neurons and glial cells embedded within the submucosal layer of the , forming a major component of the that regulates local mucosal functions including , absorption, blood flow, and epithelial permeability. This plexus enables intrinsic control of gastrointestinal through sensory detection of luminal contents and coordination of effector responses, independent of input. Named after German anatomist Georg Meissner, who first described it in 1857 based on histological observations in intestines, the submucosal plexus was initially identified as a distinct ganglionic structure separate from the . In humans and larger mammals, it comprises two interconnected layers—an inner submucosal plexus (traditional Meissner's) adjacent to the mucosa and an outer submucosal plexus (also called Henle's or Schabadasch's)—with extensive neural links to the overlying and mucosal . In contrast, smaller laboratory animals like typically feature a single layer of ganglia. Structurally, it consists of small ganglia linked by nerve fiber bundles, housing a diverse population of neurons with a higher glial-to-neuron in humans (1.3–1.9 in the inner layer and 5.9–7.0 in the outer) compared to species like the (0.8–1.0). The primary functions of the submucosal plexus center on mucosal regulation, including secretomotor control of glandular secretions from crypts of Lieberkühn, modulation of nutrient and absorption, and adjustment of local to support barrier integrity. It mediates local reflexes, such as those triggered by mechanosensitive or chemosensitive stimuli in the lumen, via intrinsic primary afferent neurons that within its ganglia. Key neuronal subtypes include secretomotor neurons for direct glandular stimulation, non-cholinergic neurons expressing (VIP) for and inhibition of secretion, and multifunctional cells that integrate sensory input with effector outputs. Nitrergic neurons are rare, and the plexus lacks direct vagal efferent innervation, underscoring its autonomous role. Notably, the submucosal plexus exhibits regional variations, with denser ganglia in the small and large intestines compared to the sparser distribution in the and , and it plays a role in immune modulation by interacting with and via VIP signaling, which enhances integrity to reduce permeability. Dysfunctions, such as neuronal loss or inflammation (submucosal plexitis), are implicated in disorders like and , highlighting its clinical significance.

Anatomy

Location and distribution

The submucosal plexus, also known as Meissner's plexus, is a network of neurons and glial cells situated in the layer of the gastrointestinal () tract, positioned between the and the inner circular muscle layer. As one of the two primary plexuses of the , alongside the , it contributes to the intrinsic neural control of GI functions. This plexus extends continuously from the to the throughout the GI tract, though its density and development vary regionally. It is most prominent and densely distributed in the small and large intestines, where it forms extensive ganglionated networks, while being minimal or absent in the and . The lies superficial to the and is embedded within the of the , in close association with blood vessels and lymphatic structures. Across species, the submucosal plexus exhibits variations in complexity; it is more elaborate and multilayered in larger mammals such as humans and pigs, whereas it typically consists of a single layer of smaller ganglia in like mice, rats, and guinea pigs. Visualization of the submucosal plexus relies on histological techniques, such as NADPH diaphorase staining to identify nitrergic neurons and fibers in whole-mount preparations, as well as advanced imaging methods like for detailed three-dimensional mapping of its distribution.

Structure and composition

The submucosal plexus is composed primarily of neurons and enteric glial cells, with glial cells outnumbering neurons by approximately four- to sixfold, resulting in a neuronal proportion of about 14-20% and glial cells comprising 80-86% of the total cellular makeup. Neurons in this plexus are generally smaller than those in the , with diameters typically ranging from 10-20 μm. These glial cells, often identified as S100β-positive, play essential roles in supporting neuronal function, providing insulation for nerve fibers, and modulating synaptic transmission within the network. Neuronal subtypes in the submucosal plexus include intrinsic primary afferent neurons (IPANs) that serve sensory functions by detecting changes in luminal contents, secretomotor neurons that regulate glandular , vasodilator neurons that control local blood flow, and that integrate signals across the network. These subtypes are characterized by distinct profiles, including (VIP) in secretomotor and vasodilator neurons, in sensory and excitatory pathways, and in secretomotor and signaling. In humans, the submucosal plexus features two layers—inner and outer—with glial-to-neuron ratios varying from 1.3-1.9 in the inner layer to 5.9-7.0 in the outer layer. The is structured as a network of small interconnected by fiber bundles, with each typically containing clusters of 4-20 in mammalian models such as rats, forming a lattice-like arrangement with varicose axons that facilitate local connectivity. In the human , density in the submucosal plexus varies regionally, ranging from approximately 12,000 neurons per cm² in the to 23,000 per cm² in the . This organization supports the 's position within the submucosal layer, enabling precise interactions with mucosal structures.

Function

Regulation of mucosal functions

The submucosal plexus plays a pivotal role in regulating gastrointestinal mucosal functions through localized neural circuits that coordinate , , and , ensuring efficient nutrient absorption, barrier integrity, and response to luminal stimuli. Secretomotor and vasodilator neurons within this plexus innervate epithelial cells, vascular elements, and the , integrating sensory inputs to maintain without direct oversight. Control of epithelial secretion is primarily mediated by secretomotor neurons in the submucosal plexus, which stimulate chloride and water secretion from crypt epithelial cells. These neurons, comprising (acetylcholine-releasing) and noncholinergic ( [VIP]-releasing) subtypes, activate (CFTR) channels on enterocytes, facilitating anion efflux and osmotic water movement into the lumen. This process is modulated by luminal factors such as nutrients, which trigger enterochromaffin cells to release serotonin (5-HT), activating afferent neurons that relay signals to secretomotor efferents, or pathogens, which enhance secretion to expel contaminants. Blood flow regulation involves vasodilator neurons that innervate submucosal arterioles, releasing (NO) and VIP to promote and increase mucosal . These neurons respond to local metabolic demands, enhancing oxygen and delivery to support absorption while also bolstering immune responses by facilitating leukocyte recruitment during . Reflex pathways in the submucosal plexus link sensory detection of luminal contents to this , ensuring coordinated adjustments in blood flow with secretory activity. The , a thin layer of underlying the mucosa, receives innervation from submucosal neurons that modulate its contractility to fold and unfold the mucosal surface, optimizing exposure for absorption and . Inhibitory neurons containing NO and VIP predominate, allowing relaxation to increase surface area during nutrient-rich conditions, while inputs may induce contractions for propulsion or barrier adjustments. This fine-tunes mucosal architecture in response to local needs, distinct from broader controlled elsewhere. Sensory integration occurs via intrinsic primary afferent neurons (IPANs) in the submucosal plexus, which detect changes in , osmolarity, and microbial signals through mucosal endings. These neurons respond to exposure by initiating protective reflexes, such as increased to neutralize pH, or to hyperosmolar contents by adjusting fluid balance; microbial products like or toxins activate similar pathways to modulate and immune surveillance. Such detection enables rapid, localized adaptations without extrinsic input. Autonomic modulation of the submucosal plexus involves parasympathetic inputs from the , which enhance secretomotor and vasodilator activity via preganglionic fibers synapsing on enteric neurons, and sympathetic inputs from prevertebral ganglia, which provide tonic inhibition to suppress excessive secretion and blood flow. These extrinsic influences fine-tune plexus excitability in response to systemic states, such as stress or feeding, but the plexus operates semi-autonomously through local circuits.

Neural signaling and interactions

Within the submucosal plexus, neural signaling occurs through intricate intraplexus synaptic connections, primarily involving fast excitatory transmission mediated by (ACh) acting on nicotinic receptors and slow transmission via neuropeptides such as (VIP) and , which modulate secretomotor and vasodilator responses. These synapses form on neuronal somata and dendrites, enabling local integration of sensory inputs from intrinsic primary afferent neurons (IPANs). Additionally, gap junctions facilitate electrical coupling between neurons and in the , though their prevalence is more pronounced in adjacent myenteric structures. The diversity of neurotransmitters in the submucosal plexus underpins its signaling complexity, with serotonin (5-HT) playing a pivotal role in coupling motility and secretion by activating IPANs via 5-HT3 and 5-HT4 receptors in response to mucosal stimuli, thereby initiating peristaltic and secretory reflexes. (CGRP), expressed in submucosal neurons and interganglionic fibers, contributes to sensory signaling, particularly enhancing sensation during through receptor activation and modulating intestinal motility via CGRP1 receptors. Local reflex arcs in the submucosal plexus operate through autonomous circuits independent of (CNS) input, allowing short reflexes such as those triggered by mucosal distension or stroking to elicit rapid secretomotor and vasodilator responses via IPAN activation of and motor neurons. These circuits process mechanosensory and chemosensory signals locally, bypassing extrinsic pathways for efficient gut . Interplexus coordination integrates submucosal signaling with the through ascending and descending projections, enabling synchronized motility-secretion reflexes like the peristaltic reflex, where submucosal IPANs relay sensory information to myenteric motor neurons for coordinated . Such bidirectional connections, often or peptidergic, ensure that local secretory adjustments align with broader peristaltic patterns. Extrinsic inputs further modulate submucosal signaling, with vagal afferents from the nodose ganglia mediating cephalic phase responses to initiate digestive reflexes via transmission to the nucleus tractus solitarius. Sacral parasympathetic preganglionic neurons (S1-S4) provide innervation for distal colonic control, enhancing and , while sympathetic fibers from thoracolumbar segments release norepinephrine to inhibit these functions through adrenergic receptors, exerting tonic suppression on submucosal activity.

Development

Embryonic origins

The submucosal plexus originates from enteric cells (ENCCs), a subpopulation of cells that delaminate from the vagal (adjacent to 1-7) and sacral (caudal to 24) levels of the . In mice, vagal ENCCs begin migrating into the at embryonic day 9.5 (E9.5), equivalent to approximately weeks 4-5 of in humans. These cells undergo extensive rostro-caudal migration along the developing gut axis, with vagal ENCCs primarily colonizing the and , while sacral ENCCs contribute to the . Failure of this colonization process can result in aganglionosis, as seen in conditions like Hirschsprung disease, where segments of the gut remain uninnervated. During migration, ENCCs proliferate and invade the gut , guided by key signaling pathways. The glial cell line-derived neurotrophic factor (GDNF)/RET signaling pathway is essential for ENCC , proliferation, and directed migration, with RET receptor expression on ENCCs responding to GDNF secreted by the surrounding . Transcription factors such as , which maintains identity and promotes glial differentiation, and Phox2b, critical for neuronal specification, regulate the subsequent differentiation of ENCCs into neurons and within the . These progenitors initially form a common pool that gives rise to both myenteric and submucosal neurons. Specification of the submucosal plexus occurs through a secondary process, where a of ENCCs migrates from the myenteric layer into the . In mice, this delamination begins around E13.5, shortly after initial gut colonization, leading to the formation of distinct submucosal neuronal clusters. The submucosal and myenteric plexuses thus arise from shared progenitors, but their separation ensures layered innervation of the gut wall. The timeline of submucosal plexus development varies by species due to differences in migration speed and gestation length. In mice, complete rostro-caudal colonization of the gut by ENCCs occurs by E14.5, with submucosal differentiation following rapidly. In humans, initial ENCC entry into the happens at week 4 of gestation, reaching the terminal by week 7, but full formation and maturation extend to approximately 20 weeks, preceding birth. This extended human timeline allows for more protracted refinement of neural networks compared to the compressed development in .

Postnatal maturation

Following the establishment of embryonic precursors, the submucosal plexus of the (ENS) undergoes extensive postnatal refinement to adapt to extrauterine conditions, including interactions with the and environmental cues. Postnatal maturation involves activity-dependent processes that shape neuronal networks, particularly through colonization shortly after birth. This colonization promotes neuronal survival and formation by stimulating the release of serotonin from s, which activates 5-HT4 receptors on enteric progenitors to drive and . Gut-derived (SCFAs), produced by microbial fermentation of dietary fibers, further enhance this process by influencing activity and indirectly supporting ENS circuit refinement. Additionally, (TLR) signaling, triggered by microbial ligands such as those recognized by TLR2 and TLR4, maintains specific neuronal subsets and modulates synaptic inputs, ensuring proper network integration in the submucosal plexus. A key aspect of this maturation is widespread neuronal , which sculpts functional circuits by eliminating excess generated during development. Approximately 50% of enteric in the proximal colon undergo in the early postnatal period, as evidenced by a roughly twofold reduction in numbers from postnatal day 7 to 4 weeks in mice. This is tightly regulated by , including (BDNF) and (NGF), which promote survival and inhibit death pathways in submucosal during this vulnerable window. Concomitant with neuronal , enteric in the submucosal plexus proliferate and mature to support barrier formation and modulation. Glial density increases in the first year of life, driven in part by microbiota-induced signaling that expands the glial network and enhances their neuroprotective roles. These form structural barriers around ganglia and regulate immune responses, contributing to the overall stability of submucosal circuits. This timeline aligns with postnatal changes in neuronal soma size and transmitter expression, enabling efficient sensory-motor responses. Environmental factors significantly influence this maturation trajectory. Dietary components, such as fiber-rich foods that foster SCFA production, support glial and neuronal development, while early stress exposure can disrupt circuit formation via altered vagal signaling and . Disruptions during this period, including microbiota from diet or stress, have been associated with long-term alterations in submucosal plexus function that predispose to conditions like (IBS) in adulthood.

Clinical significance

Associated disorders

The submucosal plexus is implicated in several pathological conditions characterized by its dysfunction or absence, leading to disrupted gastrointestinal regulation. is a congenital disorder marked by aganglionosis, or absence of cells, primarily affecting the submucosal and myenteric plexuses in the distal bowel, resulting from failed migration of cells during embryonic development. Mutations in the RET proto-oncogene account for approximately 50% of familial cases and 15-35% of sporadic cases, impairing formation and leading to symptoms such as chronic constipation, , and . Inflammatory bowel diseases (IBD), including and , involve submucosal neuronal loss and structural alterations in the due to chronic inflammation. These changes contribute to dysmotility, , and secretory abnormalities, with histopathological studies showing reduced neuronal in the submucosal plexus. Additionally, inflammation is associated with increased expression of (VIP) in submucosal neurons and mucosal tissues, which may exacerbate immune responses and tissue remodeling in affected regions. Irritable bowel syndrome (IBS) features altered excitability of submucosal sensory neurons, contributing to visceral and heightened perception from normal intestinal stimuli. This neuronal hyperexcitability in the submucosal plexus amplifies afferent signaling to the , underlying symptoms like and discomfort without overt or structural damage. Achalasia, a disorder of the , involves degeneration of inhibitory neurons in the , leading to impaired relaxation of the lower esophageal sphincter and absence of . This selective neuronal loss disrupts coordinated esophageal function, resulting in , , and regurgitation. Diabetic enteropathy arises from that affects the submucosal plexus, causing imbalances in mucosal secretion, absorption, and blood flow regulation in the . Hyperglycemia-induced damage to enteric neurons leads to altered release and impaired secretory responses, contributing to symptoms such as , , and bacterial overgrowth.

Research and therapeutic implications

Research into the submucosal plexus has advanced therapies, particularly enteric neural crest cell (ENCC) transplants, as a promising approach for treating by restoring aganglionic regions of the . Preclinical studies in models have demonstrated successful engraftment of transplanted ENSCs, leading to the formation of functional submucosal networks that improve gut motility and reduce disease severity. For instance, transplantation of ENSCs derived from human induced pluripotent s has shown integration into the host , promoting neuronal differentiation and network restoration in mouse models of . Neuroprotective agents, such as glial cell line-derived neurotrophic factor (GDNF) and its analogs, are being explored to mitigate neuronal loss in the submucosal plexus during (IBD). GDNF exhibits antiapoptotic effects on enteric neurons and reduces inflammation by downregulating pro-inflammatory cytokines like TNF-α and IL-1β in experimental models. In IBD, GDNF upregulates proteins, enhances intestinal epithelial barrier function, and promotes , thereby preventing submucosal neuronal degeneration. As of November 2025, research remains at the preclinical stage, with promising results in experimental models supporting further development for . Recent advancements in and transcriptomics have elucidated submucosal subtypes, identifying novel therapeutic targets such as Piezo2 channels. A 2025 single-cell sequencing study mapped the transcriptomes of submucosal , revealing two secretomotor classes and a previously unrecognized intrinsic primary afferent class, which provides a foundation for targeted interventions in disorders. These findings, combined with optogenetic techniques to manipulate neuronal activity, highlight Piezo2 in submucosal afferents as key regulators of gastrointestinal transit and colonic sensitivity. Disruption of Piezo2 signaling in preclinical models impairs mucosal mechanosensation, suggesting its modulation could alleviate visceral hypersensitivity in conditions like . Microbiome modulation through influences postnatal maturation of the submucosal plexus and reduces (IBS) symptoms by acting on submucosal afferents. enhance mucosal barrier integrity and alter enteric neuronal signaling, with studies showing downregulation of and in IBS patients and subsequent symptom relief upon supplementation. In developmental models, shapes submucosal network formation postnatally, promoting afferent maturation and reducing via the microbiota-gut-brain axis. Clinical evidence indicates modulate myenteric and submucosal neurons to improve IBS outcomes, emphasizing their role in afferent-mediated symptom control. Diagnostic tools for assessing submucosal plexus integrity include endoscopic combined with (IHC), which enables evaluation of neuronal and distribution in clinical samples. Deep biopsies via endoscopic submucosal dissection provide high-yield tissue for IHC staining of markers like HuC/D to detect plexus alterations in disorders. Additionally, functional MRI serves as an emerging tool to investigate blood flow dysregulation linked to submucosal plexus dysfunction, particularly in the context of gut-brain interactions during functional gastrointestinal disorders. These non-invasive approaches correlate regional changes with enteric neural activity, aiding in the diagnosis of plexus-related dysregulations.

History

Discovery and early descriptions

The submucosal plexus was first identified by German anatomist Georg Meissner in 1857 during microscopic examinations of the submucosa in the of rabbits, where he observed a secondary network of distinct from previously known structures. Meissner's studies involved maceration techniques using wood and acetic to prepare tissue samples, revealing a delicate of unmyelinated fibers embedded in the submucosal layer. In his 1857 publication in Zeitschrift für Rationelle Medizin, Meissner provided a detailed description of the ganglionated structure, noting clusters of 5 to 50 neuronal cell bodies with bipolar or multipolar morphologies, particularly prominent in the compared to the . This work distinguished the submucosal plexus from the , which was later described by Leopold Auerbach in 1862 as a coarser network located between the muscular layers of the intestinal wall. Advancements in early during the 1890s, including vital staining techniques pioneered by Alexander Dogiel, enabled clearer visualization of neuronal morphologies within the submucosal plexus, such as Dogiel type I and type II cells, contributing to initial understandings of its cellular composition. These discoveries occurred amid 19th-century debates on the enteric nervous system's degree of autonomy from control, highlighting the gut's intrinsic neural networks as key to local regulation of mucosal functions like and blood flow. Initially termed plexus submucosus in German histological literature, the name was later anglicized to submucosal plexus in English texts.

Modern advancements

In the late 19th and early 20th centuries, foundational physiological studies laid the groundwork for understanding the submucosal plexus's role in intestinal reflexes. Bayliss and Starling's 1899 experiments demonstrated that distension of the triggers coordinated peristaltic movements via intrinsic neural circuits, establishing the enteric nervous system's independence from central input and highlighting the role of plexuses in local regulation. Building on this, research in the mid-20th century, including electron microscopy studies in the 1960s, revealed the of submucosal ganglia and synapses. In the 1980s, John B. Furness advanced mapping in the submucosal plexus, identifying diverse neuronal populations through , including those containing , , and , which revealed the plexus's chemical coding for secretory and control in the guinea-pig . Furness's classifications established key functional subtypes, such as secretomotor neurons, influencing subsequent models of enteric signaling. As of 2025, ongoing advancements continue to build on these foundations, with techniques like refining classifications of submucosal neurons, though detailed research applications are explored elsewhere.

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