Synthesis and release of neuroactive substances by glial cells

Martin, David L.

doi:10.1002/glia.440050202

Cited by 304 publications

(182 citation statements)

References 104 publications

(144 reference statements)

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“…However, physiological understanding of neuron-to-glia versus glia-to-neuron communication pathways is still being elucidated. Astrocytes express receptors for neurotransmitters (Verkhratsky and Steinhä user, 2000;Araque et al, 2001), and they produce and release neuroactive substances (Martin, 1992). In addition, stimulation of astrocytes with a variety of neurotransmitters induces an elevation of intracellular calcium, which propagates as calcium waves to neighboring astrocytes via gap junctions (Araque et al, 2001).…”

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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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: 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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“…There is now clear evidence that glial cells express a large variety of receptors for neuropeptides, which are functionally coupled to second messenger systems [12,13]. We have recently found that ODN stimulates calcium mobilization in rat astrocytes [14].…”

Section: Introductionmentioning

confidence: 95%

The endozepine ODN stimulates polyphosphoinositide metabolism in rat astrocytes

et al. 1995

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Astrocytes synthesize a series of peptides called endozepines which act as endogenous ligands of benzodiazepine receptors. The present study demonstrates that the endozepine ODN causes a dose-dependent increase in inositoi trisphosphate and a parallel decrease in phosphatidylinositoi bisphosphate in cultured rat astrocytes. Pre-incubation of astrocytes with the phospholipase C inhibitor U 73122 or with pertussis toxin totally blocked polyphosphoinositide metabolism. These data show that, in rat astrocytes, ODN stimulates a phospholipase C coupled to a pertussis toxin-sensitive G protein.

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“…Increase in SCBF at the site of SCI correlates with improvement in the function of acutely injured spinal axons, 25,29 and glutamate signaling may play a role in modulation of blood¯ow and blood brain barrier permeability. 30 Therefore, we hypothesize that treatment with an NMDA antagonist after acute SCI would a ect axonal function by blocking NMDA receptors and reducing neurotoxicity at the injury site, and that there would be an increase in blood¯ow and a decrease in edema in the injured spinal cord. 31 ± 33 To test these hypotheses, we observed the e ects of pre-and posttreatment with MK801 on the axonal conduction, posttraumatic ischemia and cord edema by measuring evoked potentials, SCBF and cord water content, respectively, after acute compression SCI in rats.…”

Section: Introductionmentioning

confidence: 99%

Effects of MK801 on evoked potentials, spinal cord blood flow and cord edema in acute spinal cord injury in rats

Tator

1999

Spinal Cord

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Objectives: To determine whether MK801, an NMDA receptor antagonist, blocks glutamate excitotoxicity directly or via other mechanisms such as improving blood supply at the injury site in a rat model of spinal cord injury (SCI). In the present study, the e ects of pre-and posttreatment with MK801 on axonal function, spinal cord blood¯ow (SCBF) and cord water content were studied after acute SCI in rats. Methods: Somatosensory evoked potentials (SSEPs) and cerebellar evoked potentials (CEPs) were used to quantify electrophysiological function, and the hydrogen clearance technique and wet-dry weight measurements were used to measure SCBF and cord water content, respectively. Twenty rats received a 21 g clip compression injury of the cord at T1, and were then randomly and blindly allocated to either MK801 or saline groups. Each rat received an intravenous infusion of drug or saline four times during the experiment (16 min/infusion) with the ®rst infusion (MK801 3 mg/kg) beginning 8 min pre-injury, and the other infusions (MK801 1.5 mg/kg) at 1 h intervals after injury. Control experiments on uninjured rats were performed in 10 rats using the same procedure as above except the clip compression injury of the cord was omitted. Results: In the MK801 groups with or without SCI, the amplitude of the evoked potential peaks, especially the SSEPs, was signi®cantly lower than in the saline group. There were no di erences in SCBF or cord water content between the MK801 and saline groups. Conclusion: Pre-and posttreatment with MK801 inhibits evoked potentials, but does not improve SCBF or cord edema after acute compression SCI in rats. For the ®rst time it has been shown that MK801 produced a blockade of glutamate excitatory transmission in a erent pathways after SCI. Further work is required to determine whether this inhibition is reversible and related to neuroprotection and functional recovery after SCI.

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Synthesis and release of neuroactive substances by glial cells

Cited by 304 publications

References 104 publications

Role of enteric glial cells in inflammatory bowel disease

Role of enteric glial cells in inflammatory bowel disease

The endozepine ODN stimulates polyphosphoinositide metabolism in rat astrocytes

Effects of MK801 on evoked potentials, spinal cord blood flow and cord edema in acute spinal cord injury in rats

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