Cultured glial cells express the SNAP-25 analogue SNAP-23

Hepp, Régine; Perraut, Martine; Chasserot‐Golaz, Sylvette; Galli, Thierry; Aunis, Dominique; Langley, Keith; Grant, Nancy J.

doi:10.1002/(sici)1098-1136(199908)27:2<181::aid-glia8>3.0.co;2-9

Cited by 107 publications

(72 citation statements)

References 43 publications

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“…VGLUTs 1 and 2 were much less abundant in AsP than in LP-1, whereas VGLUT3 was more abundant in AsP. Additionally, astrocytes contained SNARE proteins, synaptobrevin 2, syntaxin, and SNAP-23 (Parpura et al, 1995b;Hepp et al, 1999). To assess the specificity of antibodies raised against VGLUTs (Table 1), we first performed preadsorption controls (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Although the mechanism of Ca 2ϩ -dependent release of glutamate from astrocytes is not fully defined, the protein components of the neuronal exocytotic machinery are expressed in astrocytes (Parpura et al, 1995b;Jeftinija et al, 1997;Bezzi et al, 1998;Hepp et al, 1999;Maienschein et al, 1999;Araque et al, 2000;Pasti et al, 2001). Additionally, Clostridial toxins, which cleave some of these exocytosis-related proteins, inhibit Ca 2ϩ -dependent release of glutamate from astrocytes (Jeftinija et al, 1997;Bezzi et al, 1998;Araque et al, 2000), indicating that regulated exocytosis most likely mediates glutamate release from astrocytes.…”

Section: Introductionmentioning

confidence: 99%

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Vesicular Glutamate Transporter-Dependent Glutamate Release from Astrocytes

Montana¹,

Ni²,

Sunjara³

et al. 2004

J. Neurosci.

338

353

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Astrocytes exhibit excitability based on variations of their intracellular Ca 2ϩ concentrations, which leads to glutamate release, that in turn can signal to adjacent neurons. This glutamate-mediated astrocyte-neuron signaling occurs at physiological intracellular Ca 2ϩ levels in astrocytes and includes modulation of synaptic transmission. The mechanism underlying Ca 2ϩ -dependent glutamate release from astrocytes is most likely exocytosis, because astrocytes express the protein components of the soluble N-ethyl maleimide-sensitive fusion protein attachment protein receptors complex, including synaptobrevin 2, syntaxin, and synaptosome-associated protein of 23 kDa. Although these proteins mediate Ca 2ϩ -dependent glutamate release from astrocytes, it is not well understood whether astrocytes express functional vesicular glutamate transporters (VGLUTs) that are critical for vesicle refilling. Here, we find in cultured and freshly isolated astrocytes the presence of brain-specific Na ϩ -dependent inorganic phosphate cotransporter and differentiation-associated Na ϩ -dependent inorganic phosphate cotransporter that have recently been identified as VGLUTs 1 and 2. Indirect immunocytochemistry showed a punctate pattern of VGLUT immunoreactivity throughout the entire cell body and processes, whereas pharmacological inhibition of VGLUTs abolished mechanically and agonist-evoked Ca 2ϩ -dependent glutamate release from astrocytes. Taken together, these data indicate that VGLUTs play a functional role in exocytotic glutamate release from astrocytes.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vesicular Glutamate Transporter-Dependent Glutamate Release from Astrocytes

Montana¹,

Ni²,

Sunjara³

et al. 2004

J. Neurosci.

338

353

View full text Add to dashboard Cite

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“…Moreover, ALAinduced SNAP-25 in NSC is probably associated with neuronal precursors, because SNAP-25 is absent in astrocytes in culture (Parpura et al, 1995;Jeftinija et al, 1997;Hepp et al, 1999), or expressed in only a small proportion of immature cells (Wilhelm et al, 2004). Therefore, from a mechanistic point of view, it is interesting to note that in the hippocampus, only the levels of SV-proteins (synaptophysin-1 and VAMP-2), but not of SNAP-25, are upregulated by subchronic ALA treatment.…”

Section: Discussionmentioning

confidence: 99%

Subchronic Alpha-Linolenic Acid Treatment Enhances Brain Plasticity and Exerts an Antidepressant Effect: A Versatile Potential Therapy for Stroke

Blondeau

Nguemeni

Debruyne

et al. 2009

Neuropsychopharmacol

122

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Omega-3 polyunsaturated fatty acids are known to have therapeutic potential in several neurological and psychiatric disorders. However, the molecular mechanisms of action underlying these effects are not well elucidated. We previously showed that alpha-linolenic acid (ALA) reduced ischemic brain damage after a single treatment. To follow-up this finding, we investigated whether subchronic ALA treatment promoted neuronal plasticity. Three sequential injections with a neuroprotective dose of ALA increased neurogenesis and expression of key proteins involved in synaptic functions, namely, synaptophysin-1, VAMP-2, and SNAP-25, as well as proteins supporting glutamatergic neurotransmission, namely, V-GLUT1 and V-GLUT2. These effects were correlated with an increase in brain-derived neurotrophic factor (BDNF) protein levels, both in vitro using neural stem cells and hippocampal cultures and in vivo, after subchronic ALA treatment. Given that BDNF has antidepressant activity, this led us to test whether subchronic ALA treatment could produce antidepressant-like behavior. ALA-treated mice had significantly reduced measures of depressive-like behavior compared with vehicletreated animals, suggesting another aspect of ALA treatment that could stimulate functional stroke recovery by potentially combining acute neuroprotection with long-term repair/compensatory plasticity. Indeed, three sequential injections of ALA enhanced protection, either as a pretreatment, wherein it reduced post-ischemic infarct volume 24 h after a 1-hour occlusion of the middle cerebral artery or as post-treatment therapy, wherein it augmented animal survival rates by threefold 10 days after ischemia.

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“…Several proteins of the synaptic vesicle exocytotic machinery, including the v-SNAREs VAMP2 and VAMP3, are expressed in astrocytes (28)(29)(30) or in astrocytoma-derived cell lines (31). Accordingly, immunostaining revealed high levels of VAMP2 and VAMP3 in primary astrocytes (Fig.…”

Section: Snare Proteins Are Required For Ca 2؉ -Dependent D-serine Rementioning

confidence: 93%

Glutamate receptor activation triggers a calcium-dependent and SNARE protein-dependent release of the gliotransmitter D-serine

Mothet

Pollegioni

Ouanounou

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

400

350

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The gliotransmitter D-serine is released upon (S)-␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid͞kainate and metabotropic glutamate receptor stimulation, but the mechanisms involved are unknown. Here, by using a highly sensitive bioassay to continuously monitor extracellular D-serine levels, we have investigated the pathways used in its release. We reveal that D-serine release is inhibited by removal of extracellular calcium and augmented by increasing extracellular calcium or after treatment with the Ca 2؉ ionophore A23187. Furthermore, release of the amino acid is considerably reduced after depletion of thapsigargin-sensitive intracellular Ca 2؉ stores or chelation of intracellular Ca 2؉ with 1,2-bis(2-aminophenoxy)ethane-N,N,N ,N -tetraacetate-acetoxymethyl ester. Interestingly, D-serine release also was markedly reduced by concanamycin A, a vacuolar-type H ؉ -ATPase inhibitor, indicating a role for the vesicular proton gradient in the transmitter storage͞release. In addition, agonist-evoked D-serine release was sensitive to tetanus neurotoxin. Finally, immunocytochemical and sucrose density gradient analysis revealed that a large fraction of D-serine colocalized with synaptobrevin͞VAMP2, suggesting that it is stored in VAMP2-bearing vesicles. In summary, our study reveals the cellular mechanisms subserving D-serine release and highlights the importance of the glial cell exocytotic pathway in influencing CNS levels of extracellular D-serine.glia ͉ synaptobrevin ͉ D-amino acid ͉ vesicles ͉ tetanus neurotoxin A strocytes play pivotal roles in synaptic transmission by controlling transmitter diffusion and concentration in the extracellular space (1) and also by back-signaling to neurons directly through the release of neuroactive substances (2). Although glutamate and ATP are the most recognized chemical transmitters that mediate astrocyte-neuron signaling (2), other cell-cell mediators also are involved in this pathway. D-Serine has recently been identified as a major gliotransmitter in the central nervous system that serves as an endogenous ligand for the glycine site of NMDA receptors (3-6).However, many aspects regarding D-serine release still need to be addressed. Although it has been suggested that astrocytes may release D-serine, through the reverse operation of a sodiumdependent transporter (7), the precise molecular mechanisms underlying D-serine release are currently unknown. To unravel the functional consequences of D-serine-mediated astrocyte-toneuron signaling, it is essential to shed light on the mechanisms controlling the gliotransmitter storage and release pathways.For this purpose, we have devised a previously undescribed bioassay to continuously monitor the release of D-serine from cultured glial cells. In this work, we show that astrocytes and C6 glioma cells synthesize and contain a large amount of D-serine that can be released upon glutamate receptor (GluR) stimulation. Moreover, our observations demonstrate that D-serine release, evoked by glutamatergic agonists, is linked to a [Ca 2ϩ...

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Cultured glial cells express the SNAP-25 analogue SNAP-23

Cited by 107 publications

References 43 publications

Vesicular Glutamate Transporter-Dependent Glutamate Release from Astrocytes

Vesicular Glutamate Transporter-Dependent Glutamate Release from Astrocytes

Subchronic Alpha-Linolenic Acid Treatment Enhances Brain Plasticity and Exerts an Antidepressant Effect: A Versatile Potential Therapy for Stroke

Glutamate receptor activation triggers a calcium-dependent and SNARE protein-dependent release of the gliotransmitter D-serine

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