The ultrastructure of Auerbach's plexus in the guinea-pig. II. Non-neuronal elements

Cook, R. D.; Burnstock, Geoffrey

doi:10.1007/bf01181656

Cited by 111 publications

(52 citation statements)

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“…Structural support for neurons and nerve bundles is not provided by connective tissue or Schwann cells as is seen in most peripheral nerves, but rather by a unique glial cell population, the enteric glial cells (EGCs). These EGCs do not synthesize myelin (Gabella, 1971;Cook and Burnstock, 1976b;Gershon and Rothman, 1991) and greatly outnumber enteric neurons. EGCs display many morphological and molecular similarities with CNS astrocytes (Table 1), suggesting that the two cell types share common functions.…”

Section: General Descriptionmentioning

confidence: 99%

“…EGCs possess a densely integrated array of intermediate filaments (Cook and Burnstock, 1976b;Komuro et al, 1982;Gabella, 1987) rich in glial fibrillary acidic protein (GFAP) (Jessen and Mirsky, 1980) and express the calcium-binding protein S100 (Ferri et al, 1982;Bishop et al, 1985;Kobayashi et al, 1986;Scheuermann et al, 1989) and glutamine synthetase both in vitro and in vivo (Jessen and Mirsky, 1983). Although these markers distinguish EGCs from myelinating Schwann cells, they are similarly expressed by CNS astrocytes and nonmyelinating Schwann cells.…”

Section: Localization and Phenotypic Characteristics Of Egcmentioning

confidence: 99%

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Role of enteric glial cells in inflammatory bowel disease

Cabarrocas

Savidge

Liblau

2002

Glia

159

154

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Enteric glial cells (EGCs) represent an extensive but relatively poorly described cell population within the gastrointestinal tract. Accumulating data suggest that EGCs represent the morphological and functional equivalent of CNS astrocytes within the enteric nervous system (ENS). The EGC network has trophic and protective functions toward enteric neurons and is fully implicated in the integration and the modulation of neuronal activities. Moreover, EGCs seem to be active elements of the ENS during intestinal inflammatory and immune responses, sharing with astrocytes the ability to act as antigen-presenting cells and interacting with the mucosal immune system via the expression of cytokines and cytokine receptors. Transgenic mouse systems have demonstrated that specific ablation of EGC by chemical ablation or autoimmune T-cell targeting induces an intestinal pathology that shows similarities to the early intestinal immunopathology of Crohn's disease. EGCs may also share with astrocytes the ability to regulate tissue integrity, thereby postulating that similar interactions to those observed for the blood-brain barrier may also be partly responsible for regulating mucosal and vascular permeability in the gastrointestinal tract. Disruption of the EGC network in Crohn's disease patients may represent one possible cause for the enhanced mucosal permeability state and vascular dysfunction that are thought to favor mucosal inflammation. GLIA 41:81-93, 2003.

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Section: General Descriptionmentioning

confidence: 99%

Section: Localization and Phenotypic Characteristics Of Egcmentioning

confidence: 99%

Role of enteric glial cells in inflammatory bowel disease

Cabarrocas

Savidge

Liblau

2002

Glia

159

154

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“…For example, the ENS lacks both internal collagen and Schwann cells. Structural support for the neural elements of the ENS is derived from cells that resemble astrocytes and have been called enteric glia (Gabella, 1971;Cook and Burnstock, 1976;Gershon and Rothman, 1991). Despite its special properties, the ENS is derived, as are other peripheral ganglia, from the neural crest .…”

Section: Introductionmentioning

confidence: 99%

Colonization of the bowel by neural crest‐derived cells re‐migrating from foregut backtransplanted to vagal or sacral regions of host embryos

Rothman

Douarin

Fontaine-Pérus

et al. 1993

Developmental Dynamics

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The enteric nervous system (ENS) in avian embryos is formed by cells that migrate to the bowel from vagal and sacral regions of the neural crest. Experiments were carried out to evaluate the developmental potential of crest-derived cells at the time they colonize the gut. Backtransplantation of E4 quail foregut (or control aneuronal hindgut) was used to determine whether crest-derived cells that have previously colonized the bowel are capable of following defined neural crest migration pathways in host embryos. Vagal and sacral, but not truncal, backgrafts provided donor cells for the host's bowel. These cells were immunostained by the neural crest marker, NC-1, restricted to the ENS, and appeared only when foregut was backgrafted; therefore, they were crest-derived. In order for cells to migrate to the host's bowel, backgrafts evidently had to be located in the vicinity of the neuraxis at the time crest-derived cells exited from them. When vagal grafts moved away from the neuraxis, crest-derived donor cells colonized cephalic ganglia and the vagus nerves near the grafts; however, such cells did not migrate down the vagi to the host's gut. Sacral backgrafts provided crestderived cells for the bowel only if the donor gut was transplanted prior to the formation of somite 28, at the level of the disappearing primitive streak. Cells from vagal backgrafts were capable of reaching the host's cloaca, but backgrafts placed at a sacral level colonized only the postumbilical bowel. In addition, donor cells proliferated extensively within the host's gut. Whenever the host's gut was colonized, donor crest-derived cells were also found in non-enteric targets including nerves, cephalic (vagal backgrafts), or sympathetic (sacral backgrafts) ganglia; however, donor cells did not form ectomesenchyme or melanocytes. These data suggest that (i) crest-derived cells that have colonized the bowel remain capable of re-migrating and following defined neural crest migration pathways in host embryos; (ii) remigrating cells must enter these pathways at their start; (iii) the gut stimulates the proliferation of enteric crest-derived cells; (iv) vagal crest-derived cells can follow sacral pathways to reach enteric, Remak's, or sympathetic ganglia; and (v) the migration of crest-derived cells within the gut is determined more by the route they follow to reach the bowel than by their level of origin in the neural crest. 0 1993 Wiley-Liss, Inc.

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“…It has characteristics that make it in many ways more similar to the brain than other autonomic ganglia, including the compact organization of neural and glial elements, absence of collagen, and paucity of extracellular space (GABELLA, 1972). Enteric glial cells resemble brain astroglia morphologically (COOK and BURNSTOCK, 1976), and share biochemical features, e.g., fibrillary acidic protein is immunologically specific for astrocytes both in the central and enteric nervous system (JESSEN and MIRSKY, 1980). Most of the putative neurotransmitters in the brain have been implicated as neurotransmitters in enteric ganglia.…”

Section: Discussionmentioning

confidence: 99%