Electrophysiologic and molecular properties of cultured enteric glia

Broussard, Delma L.; Bannerman, Peter; Tang, Cha‐Min; Hardy, Margaret H.; Pleasure, David E

doi:10.1002/jnr.490340104

Cited by 40 publications

(23 citation statements)

References 36 publications

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“…A small number of EGCs in the myenteric plexus are, however, positive, suggesting that only a subpopulation of EGCs express an astrocyte-specific GFAP isoform, although the functional significance of this observation has yet to be determined. Electrophysiological studies have also revealed heterogeneity among EGCs by demonstrating the presence of a voltage-gated tetrodotoxin-sensitive Na ϩ channel in a subpopulation of EGCs (Broussard et al, 1993;Hanani et al, 2000). The physiological significance of a voltagegated Na ϩ channel function in a small percentage of EGCs remains unclear as these cells are largely electrically inert.…”

Section: Egc Heterogeneity and Enteric Glial Networkmentioning

confidence: 99%

“…Interestingly, EGCs share these phenotypic and functional properties with astrocytes. Indeed, EGCs express voltage-activated inward and outward potassium channels (Broussard et al, 1993;Hanani et al, 2000), and electrophysiological studies have demonstrated voltage-gated potassium currents in isolated EGCs (Broussard et al, 1993). Furthermore, passive currents have been observed among gap junction-coupled EGCs in isolated ganglia (Hanani et al, 2000).…”

Section: Neuroprotective and Neuromodulatory Functions Of Egcmentioning

confidence: 99%

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Role of enteric glial cells in inflammatory bowel disease

Cabarrocas

Savidge

Liblau

2002

Glia

160

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: Egc Heterogeneity and Enteric Glial Networkmentioning

confidence: 99%

Section: Neuroprotective and Neuromodulatory Functions Of Egcmentioning

confidence: 99%

Role of enteric glial cells in inflammatory bowel disease

Cabarrocas

Savidge

Liblau

2002

Glia

160

154

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“…The expression of trophic factors by enteric glia has not been described; however, it was demonstrated that exogenous bFGF can increase the electrophysiological properties of cultured enteric glia (Broussard et al, 1993). bFGF immunoreactivity in the enteric glia described in the present study suggests a paracrine trophic action of bFGF on the enteric neurons.…”

Section: Discussionmentioning

confidence: 79%

“…The role of neurotrophic factors in neuronal development and maintenance is well established, and investigations of their actions in the enteric nervous system have been carried out (Mulholland et al, 1992(Mulholland et al, , 1994Broussard et al, 1993;Kobayashi et al, 1994;Schafer et al, 1995). However, the presence of growth factors in the enteric nervous system has not been demonstrated.…”

mentioning

confidence: 98%

Basic fibroblast growth factor, neurofilament, and glial fibrillary acidic protein immunoreactivities in the myenteric plexus of the rat esophagus and colon

Chadi

Gomide

Souza

et al. 2004

Journal of Morphology

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The enteric nervous system consists of a number of interconnected networks of neuronal cell bodies and fibers as well as satellite cells, the enteric glia. Basic fibroblast growth factor (bFGF) is a mitogen for a variety of mesodermal and neuroectodermal-derived cells and its presence has been described in many tissues. The present work employs immunohistochemistry to analyze neurons and glial cells in the esophageal and colic enteric plexus of the Wistar rat for neurofilament (NF) and glial fibrillary acidic proteins (GFAP) immunoreactivity as well as bFGF immunoreactivity in these cells. Rats were processed for immunohistochemistry; the distal esophagus and colon were opened and their myenteric plexuses were processed as whole-mount preparations. The membranes were immunostained for visualization of NF, GFAP, and bFGF. NF immunoreactivity was seen in neuronal cell bodies of esophageal and colic enteric ganglia. GFAP-immunoreactive enteric glial cells and processes were present in the esophageal and colic enteric plexuses surrounding neuronal cell bodies and axons. A dense net of GFAP-immunoreactive processes was seen in the ganglia and connecting strands of the myenteric plexus. bFGF immunoreactivity was observed in the cytoplasm of the majority of the neurons in the enteric ganglia of esophagus and colon. The two-color immunoperoxidase and immunofluorescence methods revealed bFGF immunoreactivity also in the nucleus of GFAP-positive enteric glial cells. The results suggest that immunohistochemical localization of NF and GFAP may be an important tool in the study of the plasticity in the enteric nervous system. The presence of bFGF in neurons and glia of the myenteric plexus of the esophagus and the colon indicates that this neurotrophic factor may exert autocrine and paracrine actions in the enteric nervous system.

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“…To exclude any potential contamination by glia cells, coverslips were superfused with KCl (55 mM) at the end of the experiments, and cells were excluded if intracellular Ca 2+ did not increase. 17 In this study, n equals the number of neurons examined. At least four coverslips were used for each experimental condition.…”

Section: Discussionmentioning

confidence: 99%

Glutamate-induced Calcium Transients in Rat Neurons of the Dorsal Motor Nucleus of the Vagus

Ammori

Zhang

Newman

et al. 2007

Journal of Gastrointestinal Surgery

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The dorsal motor nucleus of the vagus (DMNV) integrates peripheral and central signals and sends efferent output to the gastrointestinal system. Glutamate, the major excitatory neurotransmitter of the central nervous system, causes increases in intracellular calcium in DMNV neurons. The mechanisms by which glutamate activates calcium signaling in the DMNV were examined. DMNV neurons were isolated from neonatal rat brainstem using microdissection and enzymatic digestion. Exposure to glutamate caused intracellular Ca(2+) increments in greater than 80% of cells. Removal of extracellular Ca(2+) abolished intracellular Ca(2+) transients. Kynurenic acid, a nonspecific glutamate receptor antagonist, abolished intracellular Ca(2+) transients. Exposure to glutamate while blocking AMPA receptors with GYKI 52466 abolished the Ca(2+) response. Exposure to (S)AMPA, an AMPA receptor agonist, caused intracellular Ca(2+) increments in 97% of cells. Activation and antagonism of NMDA and kainate receptors produced no changes compared to control experiments. NiCl, a nonspecific Ca(2+) channel blocker, abolished intracellular Ca(2+) transients. Blocking T-type Ca(2+) channels with mibefradil abolished the Ca(2+) response in 76% of cells. Blockade of L-type and N-type Ca(2+) channels did not affect the Ca(2+) response. Glutamate mediates intracellular Ca(2+) currents in DMNV neurons via the AMPA receptor and T-type Ca(2+) channels, allowing influx of extracellular Ca(2+).

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Electrophysiologic and molecular properties of cultured enteric glia

Cited by 40 publications

References 36 publications

Role of enteric glial cells in inflammatory bowel disease

Role of enteric glial cells in inflammatory bowel disease

Basic fibroblast growth factor, neurofilament, and glial fibrillary acidic protein immunoreactivities in the myenteric plexus of the rat esophagus and colon

Glutamate-induced Calcium Transients in Rat Neurons of the Dorsal Motor Nucleus of the Vagus

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