Is astrocyte calcium signaling relevant for synaptic plasticity?

Achour, Sarrah Ben; Pont-Lezica, Lorena; Béchade, Catherine; Pascual, Olivier

doi:10.1017/s1740925x10000207

Cited by 38 publications

(22 citation statements)

References 128 publications

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“…Astrocytes express many ion channels and receptors that allow increases in cytosolic Ca 2+ concentration. These include voltage-gated calcium channels (VGCCs), GPCR mediated Ca 2+ release from ER, transient receptor potential (TRP) channels [23, 24, 25]. Among them, GPCR-mediated Ca 2+ increase is the most accepted mechanism for astrocytic Ca 2+ signaling.…”

Section: Discussionmentioning

confidence: 99%

Ca²⁺ Entry is Required for Mechanical Stimulation-induced ATP Release from Astrocyte

et al. 2015

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Astrocytes and neurons are inseparable partners in the brain. Neurotransmitters released from neurons activate corresponding G protein-coupled receptors (GPCR) expressed in astrocytes, resulting in release of gliotransmitters such as glutamate, D-serine, and ATP. These gliotransmitters in turn influence neuronal excitability and synaptic activities. Among these gliotransmitters, ATP regulates the level of network excitability and is critically involved in sleep homeostasis and astrocytic Ca2+ oscillations. ATP is known to be released from astrocytes by Ca2+-dependent manner. However, the precise source of Ca2+, whether it is Ca2+ entry from outside of cell or from the intracellular store, is still not clear yet. Here, we performed sniffer patch to detect ATP release from astrocyte by using various stimulation. We found that ATP was not released from astrocyte when Ca2+ was released from intracellular stores by activation of Gαq-coupled GPCR including PAR1, P2YR, and B2R. More importantly, mechanical stimulation (MS)-induced ATP release from astrocyte was eliminated when external Ca2+ was omitted. Our results suggest that Ca2+ entry, but not release from intracellular Ca2+ store, is critical for MS-induced ATP release from astrocyte.

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Section: Discussionmentioning

confidence: 99%

Ca²⁺ Entry is Required for Mechanical Stimulation-induced ATP Release from Astrocyte

et al. 2015

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“…Ca 2+ responses are of interest because intracellular Ca 2+ is a key messenger in astrocytic communication and because enzymes that synthesize the vasoactive substances responsible for neurovascular coupling are Ca 2+ -dependent (1,4). Neuronal activity releases glutamate at synapses and activates metabotropic glutamate receptors on astrocytes, and this activation can be monitored by imaging cytosolic Ca 2+ changes (11). Astrocytic Ca 2+ responses are often reported to evolve on a slow (seconds) time scale, which is too slow to account for activity-dependent increases in CBF (8,10,12,13).…”

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confidence: 99%

Rapid stimulus-evoked astrocyte Ca ²⁺ elevations and hemodynamic responses in mouse somatosensory cortex in vivo

Lind

Brazhe

Jessen

et al. 2013

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

164

197

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Increased neuron and astrocyte activity triggers increased brain blood flow, but controversy exists over whether stimulationinduced changes in astrocyte activity are rapid and widespread enough to contribute to brain blood flow control. Here, we provide evidence for stimulus-evoked Ca 2+ elevations with rapid onset and short duration in a large proportion of cortical astrocytes in the adult mouse somatosensory cortex. Our improved detection of the fast Ca 2+ signals is due to a signal-enhancing analysis of the Ca 2+ activity. The rapid stimulation-evoked Ca 2+ increases identified in astrocyte somas, processes, and end-feet preceded local vasodilatation. Fast Ca 2+ responses in both neurons and astrocytes correlated with synaptic activity, but only the astrocytic responses correlated with the hemodynamic shifts. These data establish that a large proportion of cortical astrocytes have brief Ca 2+ responses with a rapid onset in vivo, fast enough to initiate hemodynamic responses or influence synaptic activity. and associated astrocytes, which causes fluctuations in cerebral blood flow (CBF) (1-5). Astrocytes are ideally situated for controlling activity-dependent increases in CBF because they closely associate with synapses and contact blood vessels with their end-feet (1, 6). Whether or not astrocytic Ca 2+ responses develop often or rapidly enough to account for vascular signals in vivo is still controversial (7-10). Ca 2+ responses are of interest because intracellular Ca 2+ is a key messenger in astrocytic communication and because enzymes that synthesize the vasoactive substances responsible for neurovascular coupling are Ca 2+ -dependent (1, 4). Neuronal activity releases glutamate at synapses and activates metabotropic glutamate receptors on astrocytes, and this activation can be monitored by imaging cytosolic Ca 2+ changes (11). Astrocytic Ca 2+ responses are often reported to evolve on a slow (seconds) time scale, which is too slow to account for activity-dependent increases in CBF (8,10,12,13). Furthermore, uncaging of Ca 2+ in astrocytes triggers vascular responses in brain slices through specific Ca 2+ -dependent pathways with a protracted time course (14, 15). More recently, stimulation of single presynaptic neurons in hippocampal slices was shown to evoke fast, brief, local Ca 2+ elevations in astrocytic processes that were essential for local synaptic functioning in the adult brain (16,17). This work prompted us to reexamine the characteristics of fast, brief astrocytic Ca 2+ signals in vivo with special regard to neurovascular coupling, i.e., the association between local increases in neural activity and the concomitant rise in local blood flow, which constitutes the physiological basis for functional neuroimaging.Here, we describe how a previously undescribed method of analysis enabled us to provide evidence for fast Ca 2+ responses in a main fraction of astrocytes in mouse whisker barrel cortical layers II/III in response to somatosensory stimulation. The astrocytic Ca 2+ responses were brief en...

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“…From a computational modeling point of view, this is equivalent to controlling the effect of Ca 2+ in astrocytes by genetic engineering [15] and by a calcium clamp [2] in order to study the effects of astrocytic Ca 2+ on synaptic plasticity. A better understanding, through a variety of approaches, of calcium dynamics, signaling and gliotransmitter release is necessary for settling the aforementioned debate [80]. Here we have taken a computational approach and concluded that the astrocytic Ca 2+ does contribute to synaptic augmentation at the time scale of the order of seconds, for the given mathematical framework.…”

Section: Discussionmentioning

confidence: 99%

A mathematical model of the tripartite synapse: astrocyte-induced synaptic plasticity

Tewari

Majumdar

2012

J Biol Phys

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In this paper, we present a biologically detailed mathematical model of tripartite synapses, where astrocytes modulate short-term synaptic plasticity. The model consists of a pre-synaptic bouton, a post-synaptic dendritic spine-head, a synaptic cleft and a peri-synaptic astrocyte controlling Ca(2 + ) dynamics inside the synaptic bouton. This in turn controls glutamate release dynamics in the cleft. As a consequence of this, glutamate concentration in the cleft has been modeled, in which glutamate reuptake by astrocytes has also been incorporated. Finally, dendritic spine-head dynamics has been modeled. As an application, this model clearly shows synaptic potentiation in the hippocampal region, i.e., astrocyte Ca(2 + ) mediates synaptic plasticity, which is in conformity with the majority of the recent findings (Perea and Araque (Science 317, 1083-1086, 2007); Henneberger et al. (Nature 463, 232-236, 2010); Navarrete et al. (PLoS Biol. 10, e1001259, 2012)).

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Is astrocyte calcium signaling relevant for synaptic plasticity?

Cited by 38 publications

References 128 publications

Ca²⁺ Entry is Required for Mechanical Stimulation-induced ATP Release from Astrocyte

Ca²⁺ Entry is Required for Mechanical Stimulation-induced ATP Release from Astrocyte

Rapid stimulus-evoked astrocyte Ca ²⁺ elevations and hemodynamic responses in mouse somatosensory cortex in vivo

A mathematical model of the tripartite synapse: astrocyte-induced synaptic plasticity

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Is astrocyte calcium signaling relevant for synaptic plasticity?

Cited by 38 publications

References 128 publications

Ca2+ Entry is Required for Mechanical Stimulation-induced ATP Release from Astrocyte

Ca2+ Entry is Required for Mechanical Stimulation-induced ATP Release from Astrocyte

Rapid stimulus-evoked astrocyte Ca 2+ elevations and hemodynamic responses in mouse somatosensory cortex in vivo

A mathematical model of the tripartite synapse: astrocyte-induced synaptic plasticity

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Ca²⁺ Entry is Required for Mechanical Stimulation-induced ATP Release from Astrocyte

Ca²⁺ Entry is Required for Mechanical Stimulation-induced ATP Release from Astrocyte

Rapid stimulus-evoked astrocyte Ca ²⁺ elevations and hemodynamic responses in mouse somatosensory cortex in vivo