Target cell-specific modulation of neuronal activity by astrocytes

Kozlov, Andrei S.; Angulo, Marı́a Cecilia; Audinat, Etienne; Charpak, Serge

doi:10.1073/pnas.0603741103

Cited by 200 publications

(232 citation statements)

References 46 publications

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“…Since the current response evoked by local photolysis was much smaller than the one induced by wide-field illumination, the increase in neuronal activity probably was not large enough to evoke measurable calcium transients in the mitral cell dendrite. Olfactory bulb astrocytes express P2Y 1 receptors and modulate neuronal excitability as well as synaptic transmission in the olfactory bulb [16,35], suggesting the possibility that the increase in neuronal activity upon photorelease of ATP is a consequence of ATP-mediated activation of astrocytes. However, Kozlov et al [35] described a GABAergic inhibitory effect of astrocytes on mitral cells, in contrast to the glutamatergic excitatory effect shown here.…”

Section: Mechanism Of Atp-mediated Stimulation Of Network Activitymentioning

confidence: 99%

“…Olfactory bulb astrocytes express P2Y 1 receptors and modulate neuronal excitability as well as synaptic transmission in the olfactory bulb [16,35], suggesting the possibility that the increase in neuronal activity upon photorelease of ATP is a consequence of ATP-mediated activation of astrocytes. However, Kozlov et al [35] described a GABAergic inhibitory effect of astrocytes on mitral cells, in contrast to the glutamatergic excitatory effect shown here. In addition, TTX, which does not affect astrocyte performance, strongly suppressed the P2Y 1 receptor-mediated enhancement of network activity, rendering astrocytes as less likely candidates for the ATP-dependent effect measured in the present study.…”

Section: Mechanism Of Atp-mediated Stimulation Of Network Activitymentioning

confidence: 99%

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P2Y1 receptor activation by photolysis of caged ATP enhances neuronal network activity in the developing olfactory bulb

Fischer

Rotermund

Lohr

et al. 2011

Purinergic Signalling

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It has recently been shown that adenosine-5′-triphosphate (ATP) is released together with glutamate from sensory axons in the olfactory bulb, where it stimulates calcium signaling in glial cells, while responses in identified neurons to ATP have not been recorded in the olfactory bulb yet. We used photolysis of caged ATP to elicit a rapid rise in ATP and measured whole-cell current responses in mitral cells, the output neurons of the olfactory bulb, in acute mouse brain slices. Wide-field photolysis of caged ATP evoked an increase in synaptic inputs in mitral cells, indicating an ATP-dependent increase in network activity. The increase in synaptic activity was accompanied by calcium transients in the dendritic tuft of the mitral cell, as measured by confocal calcium imaging. The stimulating effect of ATP on the network activity could be mimicked by photo release of caged adenosine 5′-diphosphate, and was inhibited by the P2Y 1 receptor antagonist MRS 2179. Local photolysis of caged ATP in the glomerulus innervated by the dendritic tuft of the recorded mitral cell elicited currents similar to those evoked by wide-field illumination. The results indicate that activation of P2Y 1 receptors in the glomerulus can stimulate network activity in the olfactory bulb.

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Section: Mechanism Of Atp-mediated Stimulation Of Network Activitymentioning

confidence: 99%

Section: Mechanism Of Atp-mediated Stimulation Of Network Activitymentioning

confidence: 99%

P2Y1 receptor activation by photolysis of caged ATP enhances neuronal network activity in the developing olfactory bulb

Fischer

Rotermund

Lohr

et al. 2011

Purinergic Signalling

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“…and CA3 of the hippocampus (Angulo et al, 2004;Fellin et al, 2004;Kang et al, 2005;Perea and Araque, 2005;Tian et al, 2005), the thalamus (Parri et al, 2001), the olfactory bulb (Kozlov et al, 2006), the nucleus accumbens (D'Ascenzo et al, 2007), and the cortex (this study), it is likely that they are a general property of the nervous system.…”

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confidence: 99%

Enhanced Astrocytic Ca²⁺Signals Contribute to Neuronal Excitotoxicity after Status Epilepticus

Ding¹,

Fellin²,

Zhu³

et al. 2007

J. Neurosci.

247

260

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Status epilepticus (SE), an unremitting seizure, is known to cause a variety of traumatic responses including delayed neuronal death and later cognitive decline. Although excitotoxicity has been implicated in this delayed process, the cellular mechanisms are unclear. Because our previous brain slice studies have shown that chemically induced epileptiform activity can lead to elevated astrocytic Ca 2ϩ signaling and because these signals are able to induce the release of the excitotoxic transmitter glutamate from these glia, we asked whether astrocytes are activated during status epilepticus and whether they contribute to delayed neuronal death in vivo. Using two-photon microscopy in vivo, we show that status epilepticus enhances astrocytic Ca 2ϩ signals for 3 d and that the period of elevated glial Ca 2ϩ signaling is correlated with the period of delayed neuronal death. To ask whether astrocytes contribute to delayed neuronal death, we first administered antagonists which inhibit gliotransmission: MPEP [2-methyl-6-(phenylethynyl)pyridine], a metabotropic glutamate receptor 5 antagonist that blocks astrocytic Ca 2ϩ signals in vivo, and ifenprodil, an NMDA receptor antagonist that reduces the actions of glial-derived glutamate. Administration of these antagonists after SE provided significant neuronal protection raising the potential for a glial contribution to neuronal death. To test this glial hypothesis directly, we loaded Ca 2ϩ chelators selectively into astrocytes after status epilepticus. We demonstrate that the selective attenuation of glial Ca 2ϩ signals leads to neuronal protection. These observations support neurotoxic roles for astrocytic gliotransmission in pathological conditions and identify this process as a novel therapeutic target.

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“…[Ca 2ϩ ] i increases, between a few nanomolar (11) and tens of micromolar (12) triggered by flash photolysis of caged Ca 2ϩ or pharmacological means (13), trigger release of transmitters from astrocytes into the extracellular space, which may then activate receptors on other nearby cells, including neurons. For instance, recent experiments suggest that [Ca 2ϩ ] i increases within single astrocytes can release glutamate, which activates extrasynaptic NMDA receptors on neurons (14,15), leading to synchrony (14). In addition in the olfactory bulb, astrocytes release GABA to cause inhibition of mitral cells (15).…”

mentioning

confidence: 99%

Two forms of single-vesicle astrocyte exocytosis imaged with total internal reflection fluorescence microscopy

Bowser

Khakh²

2007

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

144

168

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Transmitters such as glutamate and ATP are released from brain astrocytes. Several pathways for their release have been proposed, including exocytosis. In the present study we sought to measure exocytosis from astrocytes with single vesicle imaging methods using synaptopHlourin (SpH) as an optical reporter. We imaged single SpH-laden vesicles with total internal reflection fluorescence (TIRF) microscopy. We observed spontaneous, as well as evoked, single-vesicle exocytosis events. Analysis of the kinetics and spatial spread associated with these events indicated two discernible forms of single vesicle exocytosis. One form, constituting Ϸ40% of the spontaneous events, was akin to kiss-and-run vesicle fusion and captured a mobile proton buffer from the extracellular medium. The other form seems to represent full vesicle fusion, constitutes Ϸ60% of the spontaneous events, and is associated with complete mixing of the vesicle and plasma membranes. Activation of calcium-mobilizing receptors on the astrocyte surface selected between the different forms of exocytosis. These data provide evidence for two forms of simultaneously occurring singlevesicle exocytosis events in astrocytes, and also suggest that SpH imaging and TIRF microscopy is useful to study the mechanisms of astrocyte transmitter release.imaging ͉ calcium ͉ ATP

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Target cell-specific modulation of neuronal activity by astrocytes

Cited by 200 publications

References 46 publications

P2Y1 receptor activation by photolysis of caged ATP enhances neuronal network activity in the developing olfactory bulb

P2Y1 receptor activation by photolysis of caged ATP enhances neuronal network activity in the developing olfactory bulb

Enhanced Astrocytic Ca²⁺Signals Contribute to Neuronal Excitotoxicity after Status Epilepticus

Two forms of single-vesicle astrocyte exocytosis imaged with total internal reflection fluorescence microscopy

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Target cell-specific modulation of neuronal activity by astrocytes

Cited by 200 publications

References 46 publications

P2Y1 receptor activation by photolysis of caged ATP enhances neuronal network activity in the developing olfactory bulb

P2Y1 receptor activation by photolysis of caged ATP enhances neuronal network activity in the developing olfactory bulb

Enhanced Astrocytic Ca2+Signals Contribute to Neuronal Excitotoxicity after Status Epilepticus

Two forms of single-vesicle astrocyte exocytosis imaged with total internal reflection fluorescence microscopy

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Enhanced Astrocytic Ca²⁺Signals Contribute to Neuronal Excitotoxicity after Status Epilepticus