GFAP‐positive hippocampal astrocytes in situ respond to glutamatergic neuroligands with increases in [Ca<sup>2+</sup>]<sub>i</sub>

Porter, James T.; McCarthy, Ken D.

doi:10.1002/glia.440130204

Cited by 192 publications

(141 citation statements)

References 52 publications

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“…These observations indicate that glutamate released from depolarized nerve terminals contributes to the correlation of astrocyte Ca 2ϩ activity. This view is also in agreement with data on the functional expression of NMDA and non-NMDA receptors in astrocytes (Porter and McCarthy, 1995;Schipke et al, 2001).…”

supporting

confidence: 92%

“…Because the removal of extracellular Ca 2ϩ might deplete intracellular Ca 2ϩ stores, we evaluated the levels of Ca 2ϩ in intracellular stores of astrocytes perfused with nominally Ca 2ϩ -free ACSF by activating IP 3 and ryanodine receptors. To activate IP 3 -mediated Ca 2ϩ release from intracellular stores, we used the metabotropic glutamate receptor agonist t-ACPD (Porter and McCarthy, 1995). Addition of t-ACPD (5 M) to Ca 2ϩ -free ACSF triggered a transient increase of [Ca 2ϩ ] i in 52 of 54 identified astrocytes (two slices from two animals) (Fig.…”

Section: G)mentioning

confidence: 99%

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Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

et al. 2002

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Spontaneous neuronal activity is essential to neural development. Until recently, neurons were believed to be the only excitable cells to display spontaneous activity. However, cultured astrocytes and, more recently, astrocytes in situ are now known to exhibit spontaneous Ca 2ϩ transients. Here we used Ca 2ϩ imaging of astrocytes from transgenic mice for the simultaneous monitoring of [Ca 2ϩ ] i changes in large numbers of astrocytes. We found that spontaneous activity is a common property of most brain astrocytes that is lost in response to a lesion. These spontaneous [Ca 2ϩ ] i oscillations require extracellular and intracellular Ca 2ϩ . Moreover, network analysis revealed that most astrocytes formed correlated networks of dozens of these cells, which were synchronous with both astrocytes and neurons. We found that decreasing spontaneous [Ca 2ϩ ] i transients in neurons by TTX does not alter the number of active astrocytes, although it impairs their synchronous network activity. Conversely, bicuculline-induced epileptic patterns of [Ca 2ϩ ] i transients in neurons cause an increase in the number of active astrocytes and in their network synchrony. Furthermore, activation of non-NMDA and NMDA ionotropic glutamate receptors is required to correlate astrocytic networks. These results show that spontaneous activity in astrocytes and neurons is patterned into correlated neuronal/astrocytic networks in which neuronal activity regulates the network properties of astrocytes. This network activity may be essential for neural development and synaptic plasticity.

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confidence: 92%

Section: G)mentioning

confidence: 99%

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

et al. 2002

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“…Single-cell [Ca2~j 1 recordings then demonstrated that the occurrence of oscillatory [Ca 2~]~responses by the mGluR-specific agonist correlates well with the induction of mGluRS in cultured astrocytes. It has been reported that [Ca2~Iõ scillations are also evoked in cultured astocytes by activation of ionotropic glutamate receptors (Porter and McCarthy, 1995). However, 1 S,3R-ACPD-induced [Ca2~I 1oscillations were blocked solely by the mGluR antagonist, and not by either the AMPA/kainate receptor antagonist or the NMDA receptor antagonist, and did not require calcium in the external medium.…”

Section: Discussionmentioning

confidence: 87%

The Metabotropic Glutamate Receptor mGluR5 Induces Calcium Oscillations in Cultured Astrocytes via Protein Kinase C Phosphorylation

Nakahara

Okada²,

Nakanishi

1997

Journal of Neurochemistry

133

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Abstract:The metabotropic glutamate receptor mGluR5, but not the closely related mGluRl, is expressed in cultured astrocytes, and this expression is up-regulated by specific growth factors. We investigated the capability and underlying mechanisms of mGluR5 to induce oscillatory responses of intracellular calcium concentration ([Ca 2~]) in cultured rat astrocytes. recordings indicated that an mGluR-selective agonist, (1 S,3R)-1 -aminocyclopentane-1,3-dicarboxylate (1 S,3R-ACPD), elicits [Ca2~], oscillations in good agreement with the growth factor-induced up-regulation of mGluR5 in cultured astrocytes. A protein kinase C (PKC) inhibitor, bisindolylmaleimide I, converted a 1S,3R-ACPD-mediated oscillatory response into a nonoscillatory response. In addition, the PKC activator phorbol 12-myristate 13-acetate completely abolished the [Ca2~]increase. These and other pharmacological properties of 1S,3R-ACPD-induced [Ca2~]õscillations correlate well with those of the cloned mGluR5 characterized in heterologous expression systems. Furthermore, the potential involvement of protein phosphatases in [Ca2~]õscilla-tions is suggested. The present study demonstrates that mGluR5 is capable of inducing [Ca2~] 1 oscillations in cultured astrocytes and that phosphorylation/dephosphorylation of mGluR5 is critical in [Ca 2~]oscillations, analogous to the cloned mGluR5 expressed in heterologous cell lines.

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“…(Bowman et al 2003;Conti et al 1994;Hosli and Hosli 1993;Imura et al 2006;Matthias et al 2003;Miller and Szigeti 1991;Nikcevich et al 1997;Porter and McCarthy 1995;Shao et al 1994;St-Pierre et al 2000;Swanson et al 1997;Venance et al 1998;Whitaker-Azmitia et al 1993;Zhou and Kimelberg 2001). For example, both in vitro and in vivo studies show that the expression of glutamate transporter isoforms GLT-1 and GLAST segregate to different hippocampal GFAP-positive astrocytes (Conti et al 1998;Perego et al 2000;van Landeghem et al 2006).…”

Section: Discussionmentioning

confidence: 99%

TGFβ1 and TNFα potentiate nitric oxide production in astrocyte cultures by recruiting distinct subpopulations of cells to express NOS-2

Hamby¹,

Gragnolati²,

Hewett³

et al. 2008

Neurochemistry International

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Nitric oxide (NO) synthase-2 (NOS-2), a key source of NO at sites of neuroinflammation, is induced in astrocyte cultures treated with lipopolysaccharide (LPS) plus interferon-γ (IFNγ). A recent study examining the regulation of astrocytic NOS-2 expression demonstrated that transforming growth factor-β1 (TGFβ1) potentiated LPS plus IFNγ-induced NOS-2 expression via expansion of the pool of astrocytes that express NOS-2. Results in the current report indicate that this population-based mechanism of increasing NOS-2 expression is not restricted to TGFβ1, since it also accounts for the potentiation of NO production in astrocyte cultures by tumor necrosis factor-α (TNFα). In contrast to TGFβ1, which required 24 hr preincubation for optimal potentiation of NO production, TNFα was maximally effective when added concurrently with LPS plus IFNγ. Nevertheless, under conditions that optimally potentiated NO production, both cytokines recruited similar numbers of astrocytes to express NOS-2 (% NOS-2-positive cells after LPS plus IFNγ alone or with TNFα or TGFβ1 was 9.5 ± 1.2, 25.3 ± 2.9, and 32.4 ± 3.0, respectively). Interestingly, stimulation of astrocytes in the presence of both TGFβ1 and TNFα additively increased the number of astrocytes that expressed NOS-2 protein (% NOS-2-positive cells was 61.0 ± 4.2) relative to each cytokine alone. Potentiation of NO production by either TNFα or TGFβ1 was not ablated by neutralizing antibodies to TGFβ1 or TNFα, respectively. Thus, the two cytokines act independently to recruit separate pools of astrocytes to express NOS-2. These results are consistent with the notion that astrocytes possess an innate heterogeneity with respect to responsiveness to these cytokines. KeywordsLPS; cytokines; heterogeneity; NO; iNOS; nitric oxide synthase Nitric oxide (NO) is an endogenously derived free radical gas that affects a spectrum of homeostatic and physiologic processes, including blood flow and coagulation, normal brain and heart function, and innate immunity (Belge et al. 2005;Ignarro et al. 1999;MacMicking et al. 1997;Yun et al. 1996). However, it can be harmful under certain pathophysiological conditions. Within the CNS, aberrant NO production has been linked to cerebrovascular dysfunction ( Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NO is derived from L-arginine by the catalytic action of three different NOS isoforms (Stuehr 1999). NOS-1 and -3 are constitutively expressed in neurons and endothelial cells, respectively, and thus were initially termed nNOS and eNOS. In contrast, NOS-2 is not constitutively expressed but can be induced ...

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GFAP‐positive hippocampal astrocytes in situ respond to glutamatergic neuroligands with increases in [Ca²⁺]_i

Cited by 192 publications

References 52 publications

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

The Metabotropic Glutamate Receptor mGluR5 Induces Calcium Oscillations in Cultured Astrocytes via Protein Kinase C Phosphorylation

TGFβ1 and TNFα potentiate nitric oxide production in astrocyte cultures by recruiting distinct subpopulations of cells to express NOS-2

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GFAP‐positive hippocampal astrocytes in situ respond to glutamatergic neuroligands with increases in [Ca2+]i

Cited by 192 publications

References 52 publications

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

Neuronal Activity Regulates Correlated Network Properties of Spontaneous Calcium Transients in AstrocytesIn Situ

The Metabotropic Glutamate Receptor mGluR5 Induces Calcium Oscillations in Cultured Astrocytes via Protein Kinase C Phosphorylation

TGFβ1 and TNFα potentiate nitric oxide production in astrocyte cultures by recruiting distinct subpopulations of cells to express NOS-2

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GFAP‐positive hippocampal astrocytes in situ respond to glutamatergic neuroligands with increases in [Ca²⁺]_i