Up-regulation of P2X7 receptor-immunoreactivity by in vitro ischemia on the plasma membrane of cultured rat cortical neurons

Milius, Doreen; Sperlágh, Beáta; Illéš, Peter

doi:10.1016/j.neulet.2008.09.023

Cited by 14 publications

(18 citation statements)

References 27 publications

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“…A series of functional data strongly supports the role of P2X 7 Rs in information processing in the normal and pathological nervous systems [25] . Several investigations s u g g e s t t h a t a f t e r c e r e b r a l i s c h e m i c i n j u r y, t h e extracellularly-accumulated ATP facilitates glutamate and gamma-aminobutyric acid (GABA) release from the terminals of neurons, astrocytes, and cortical microglia upon energy deprivation [3,56] .…”

Section: Activated P2x 7 Receptors Modulate Neurotransmitter Releasementioning

confidence: 79%

“…They directly participate in the metabolic impairment. OGD in mixed astrocytic/neuronal cultures selectively up-regulates P2X 7 R immunoreactivity in the plasma membrane of neurons, but not astrocytes, 12 h after ischemia [25] . Post-ischemic, time-dependent up-regulation of the P2X 7 R subtype on neurons and microglia in the MCAO model might be involved in neuronal apoptosis and tissue damage, suggesting a role of this receptor in the pathophysiology of cerebral ischemia in vivo [1,4] .…”

Section: Receptors In Cerebral Ischemiamentioning

confidence: 94%

“…Under normal conditions, P2X 7 Rs are widespread on the membranes of neurons, astrocytes, microglia, oligodendrocytes, and oligodendrocyte precursor cells, as well as Schwann cells [14,[25][26][27] , unlike the localization of P2X [1][2][3][4][5][6] receptor subtypes, which is mainly on the membranes of neurons [28] . They are especially abundant on microglia that are in a physiologically resting state, [20] , and play protective roles such as host defense and tissue repair [28] against neuronal damage [29] , suggesting that P2X 7 Rs are involved in immune functions and inflammatory responses [13] .…”

Section: Physiological Conditionsmentioning

confidence: 99%

“…There are several possible modes of ATP release: (1) damaged neurons are depolarized by the elevated extracellular K + due to impairment of the Na + -K + pump. ATP passively flows out along the electrochemical gradient through membrane channels of glial cells [23] or from the presynaptic vesicles exocytotically [35] ; (2) organelles release ATP from astroglia in a Ca 2+ -independent manner via P2X 7 R channels [25,36] ; and (3) P2X 7 Rs on activated amoeboid microglia and reactive microglia amplify the ATP signal and trigger ATP release through an autocrine process [37,38] . In short, cerebral ischemia results in a sustained progressive elevation of ATP levels in the penumbra [22,23] .…”

Section: Leading To Cell Deathmentioning

confidence: 99%

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P2X7 receptors in cerebral ischemia

Bai

2013

Neurosci. Bull.

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Cerebral ischemia is one of the most common diseases resulting in death and disability in aged people. It leads immediately to rapid energy failure, ATP depletion, and ionic imbalance, which increase extracellular ATP levels and accordingly activate P2X 7 receptors. These receptors are ATP-gated cation channels and widely distributed in nerve cells, especially in the immunocompetent cells of the brain. Currently, interest in the roles of P2X 7 receptors in ischemic brain injury is growing. In this review, we discuss recent research progress on the actions of P2X 7 receptors, their possible mechanisms in cerebral ischemia, and the potential therapeutic value of P2X 7 receptor antagonists which may provide a new target both for clinical and for research purposes.

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Section: Activated P2x 7 Receptors Modulate Neurotransmitter Releasementioning

confidence: 79%

Section: Receptors In Cerebral Ischemiamentioning

confidence: 94%

Section: Physiological Conditionsmentioning

confidence: 99%

Section: Leading To Cell Deathmentioning

confidence: 99%

See 2 more Smart Citations

P2X7 receptors in cerebral ischemia

Bai

2013

Neurosci. Bull.

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“…Oxygen-glucose deprivation (OGD) can occur in ischemia, and it is related to neuronal injury [7,25,26]. The P2X 7 receptor is involved in neuronal injury after ischemic diseases [7,17,21,27].…”

Section: Introductionmentioning

confidence: 99%

The effects of NONRATT021972 lncRNA siRNA on PC12 neuronal injury mediated by P2X7 receptor after exposure to oxygen-glucose deprivation

Zou

Xie

et al. 2016

Purinergic Signalling

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Adenosine triphosphate (ATP) participates in signal transmission by acting on P2X receptors, and the P2X 7 receptor is involved in the pathophysiological changes of ischemic injury. The PC12 cell line is a popular model system to study sympathetic neuronal function. Long noncoding RNAs (lncRNAs) are highly expressed in the nervous system and serve as regulatory RNAs. In this study, the effects of NONRATT021972 lncRNA siRNA on P2X 7 -mediated PC12 neuronal injury after exposure to oxygenglucose deprivation (OGD) were investigated. Our results showed that the viability of PC12 cells cultured with OGD or the P2X 7 agonist BzATP was significantly decreased. Treatment with NONRATT021972 siRNA reversed the decreased viability of PC12 cells under OGD conditions. The upregulated P2X 7 mRNA and protein levels in PC12 cells under OGD conditions or BzATP treatment were significantly decreased when pretreated with NONRATT021972 siRNA. Moreover, NONRATT021972 siRNA treatment effectively suppressed the increase in [Ca 2+ ] i induced by OGD or P2X 7 agonists (ATP or BzATP) in PC12 cells. Therefore, treatment with NONRATT021972 siRNA may decrease sympathetic neuronal injury induced by ischemia.

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Effects of Acute Perinatal Asphyxia in the Rat Hippocampus

et al. 2010

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In the present work, we have used a rat animal model to study the early effects of intrauterine asphyxia occurring no later than 60 min following the cesarean-delivery procedure. Transitory hypertonia accompanied by altered posture was observed in asphyxiated pups, which also showed appreciably increased lactate values in plasma and hippocampal tissues. Despite this, there was no difference in terms of either cell viability or metabolic activities such as oxidation of lactate, glucose, and glycine in the hippocampus of those fetuses submitted to perinatal asphyxia with respect to normoxic animals. Moreover, a significant decrease in glutamate, but not GABA uptake was observed in the hippocampus of asphyctic pups. Since intense ATP signaling especially through P2X(7) purinergic receptors can lead to excitotoxicity, a feature which initiates neurotransmission failure in experimental paradigms relevant to ischemia, here we assessed the expression level of the P2X(7) receptor in the paradigm of perinatal asphyxia. A three-fold increase in P2X(7) protein was transiently observed in hippocampus immediately following asphyxia. Nevertheless, further studies are needed to delineate whether the P2X(7) receptor subtype is involved in the pathogenesis, contributing to ongoing brain injury after intrapartum asphyxia. In that case, new pharmacologic intervention strategies providing neuroprotection during the reperfusion phase of injury might be identified.

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Up-regulation of P2X7 receptor-immunoreactivity by in vitro ischemia on the plasma membrane of cultured rat cortical neurons

Cited by 14 publications

References 27 publications

P2X7 receptors in cerebral ischemia

P2X7 receptors in cerebral ischemia

The effects of NONRATT021972 lncRNA siRNA on PC12 neuronal injury mediated by P2X7 receptor after exposure to oxygen-glucose deprivation

Effects of Acute Perinatal Asphyxia in the Rat Hippocampus

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