Astroglial Ca 2+ signaling is generated by the coordination of IP 3 R and store-operated Ca 2+ channels

Sakuragi, Shigeo; Niwa, Fumihiro; Oda, Yoichi; Mikoshiba, Katsuhiko; Bannai, Hiroko

doi:10.1016/j.bbrc.2017.03.096

Cited by 22 publications

(15 citation statements)

References 37 publications

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“…The molecular mechanism of maintaining Cl − ion homeostasis by astrocytes includes GABA receptor anion channels (Fraser et al, 1995) and ClC-2. Ca 2+ ion homoeostasis relies on a Na + /Ca 2+ exchanger 1-3 (NCX1-3) (Verkhratsky et al, 2012) and plasmalemmal Ca 2+ pump (PMC) and is controlled by the coordination of IP3R and store-operated Ca 2+ channels (Blaustein et al, 2002;Liu et al, 2017;Reyes et al, 2012;Sakuragi et al, 2017). Neurotransmitter homeostasis refers to glutamate, GABA, glycine, and adenosine.…”

Section: Physical Function Of Astrocytesmentioning

confidence: 99%

Morphological and functional alterations of astrocytes responding to traumatic brain injury

Cheng

Wang

Xiao

et al. 2019

Journal of Integrative Neuroscience

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Section: Physical Function Of Astrocytesmentioning

confidence: 99%

Morphological and functional alterations of astrocytes responding to traumatic brain injury

Cheng

Wang

Xiao

et al. 2019

Journal of Integrative Neuroscience

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“…The present study also showed that the store-operated calcium channel was required to release ATP after relatively mild CCI injury. The store-operated calcium channel, together with the endoplasmic reticulum, is known to be essential for astrocytes to control the intracellular calcium level (43). The pre-injury ATP value of the CCI-2-APB group was significantly higher than that of the CCI-MRS2179 group, and it was similar to that of the sham and CCI groups.…”

Section: Discussionmentioning

confidence: 77%

Massive efflux of adenosine triphosphate into the extracellular space immediately after experimental traumatic brain injury

Moro¹,

Ghavim²,

Sutton³

2021

Exp Ther Med

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The aim of the current study was to determine effects of mild traumatic brain injury (TBI), with or without blockade of purinergic ATP Y1 (P2Y1) receptors or store-operated calcium channels, on extracellular levels of ATP, glutamate, glucose and lactate. Concentrations of ATP, glutamate, glucose and lactate were measured in cerebral microdialysis samples obtained from the ipsilateral cortex and underlying hippocampus of rats with mild unilateral controlled cortical impact (CCI) or sham injury. Immediately after CCI, a large release of ATP was observed in the cortex (3.53-fold increase of pre-injury value) and hippocampus (2.97-fold increase of pre-injury value), with ATP returning to the baseline levels within 20 min post-injury and remaining stable for during the 3-h sampling period. In agreement with the results of previous studies, there was a significant increase in glutamate 20 min after CCI, which was concomitant with a decrease in extracellular glucose (20 min) and an increase in lactate (40-60 min) in both brain regions after CCI. Addition of a selective P2Y1 receptor blocker (MRS2179 ammonium salt hydrate) to the microdialysis perfusate significantly lowered pre-injury ATP and glutamate levels, and eliminated the post-CCI peaks. Addition of a blocker of store-operated calcium channels [2-aminoethoxy diphenylborinate (2-APB)] to the microdialysis perfusate significantly lowered pre-injury ATP in the hippocampus, and attenuated the post-CCI peak in both the cortex and hippocampus. 2-APB treatment significantly increased baseline glutamate levels, but the values post-injury did not differ from those in the sham group. Pre-injury glucose levels, but not lactate levels, were increased by MRS2179 and decreased by 2-APB. However, none of these treatments substantially altered the CCI-induced reduction in glucose and increase in lactate in the cortex. In conclusion, the results of the present study demonstrated that a short although extensive release of ATP immediately after experimental TBI can be significantly attenuated by blockade of P2Y1 receptors or store-operated calcium channels.

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“…Through the activation of inositol triphosphate receptor (IP3R), the endoplasmic reticulum (ER) represents the major source of calcium in astrocytes [34,35].…”

Section: Molecular Mechanisms Of the Mtcb 1 Receptor-dependent Mitochondrial Calcium Increase In Astrocytesmentioning

confidence: 99%

“…Thus, the ER mediates both cytosolic and mitochondrial cannabinoid-induced calcium increases. IP3R are the main players of metabotropic control of cytosolic calcium in astrocytes and, interestingly, they are present in MERCs[34,35,37]. To determine whether IP3R are involved in cannabinoid-mediated increase in cytosolic and/or mitochondrial calcium, we applied the IP3R antagonist 2-Aminoethoxydiphenyl borate (2APB, 100 µM,Figure 2A)to CB 1 -expressing astrocytes.…”

mentioning

confidence: 99%

Astroglial calcium transfer from endoplasmic reticulum to mitochondria determines synaptic integration

Serrat

Covelo

Kouskoff

et al. 2020

Preprint

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SummaryIntracellular calcium signaling underlies the astroglial control of synaptic transmission and plasticity. Mitochondria-endoplasmic reticulum contacts (MERCs) are key determinants of calcium dynamics, but their functional impact on astroglial regulation of brain information processing is currently unexplored. We found that the activation of astrocyte mitochondrial-associated CB1 receptors (mtCB1) determines MERCs-dependent intracellular calcium signaling and synaptic integration. The stimulation of mtCB1 receptors promotes calcium transfer from the endoplasmic reticulum to mitochondria through specific mechanisms regulating the activity of the mitochondrial calcium uniporter (MCU) channel. Physiologically, mtCB1-dependent mitochondrial calcium uptake determines the precise dynamics of cytosolic calcium events in astrocytes upon endocannabinoid mobilization. Accordingly, electrophysiological recordings in hippocampal slices showed that genetic exclusion of mtCB1 receptors or specific astroglial MCU inhibition blocks lateral synaptic potentiation, a key example of astrocyte-dependent integration of distant synapses activity. Altogether, these data reveal an unforeseen link between astroglial MERCs and the regulation of brain network functions.

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Astroglial Ca 2+ signaling is generated by the coordination of IP 3 R and store-operated Ca 2+ channels

Cited by 22 publications

References 37 publications

Morphological and functional alterations of astrocytes responding to traumatic brain injury

Morphological and functional alterations of astrocytes responding to traumatic brain injury

Massive efflux of adenosine triphosphate into the extracellular space immediately after experimental traumatic brain injury

Astroglial calcium transfer from endoplasmic reticulum to mitochondria determines synaptic integration

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