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Cited by 89Adenosine and Purinergic SignalingNeuroscience and Neuropharmacology ResearchPain Mechanisms and Treatments

Supersensitivity of P2X7 receptors in cerebrocortical cell cultures after in vitro ischemia

Wirkner, Kerstin, Köfalvi, Attila, Fischer, Wolfgang, Günther, Albrecht, Franke, Heike, Gröger‐Arndt, Helke, Nörenberg, Wolfgang, Madarász, Emília +4 more·2005·Journal of Neurochemistry
DOI 10.1111/j.1471-4159.2005.03465.x
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Abstract

Neuronally enriched primary cerebrocortical cultures were exposed to glucose-free medium saturated with argon (in vitro ischemia) instead of oxygen (normoxia). Ischemia did not alter P2X7 receptor mRNA, although serum deprivation clearly increased it. Accordingly, P2X7 receptor immunoreactivity (IR) of microtubuline-associated protein 2 (MAP2)-IR neurons or of glial fibrillary acidic protein (GFAP)-IR astrocytes was not affected; serum deprivation augmented the P2X7 receptor IR only in the astrocytic, but not the neuronal cell population. However, ischemia markedly increased the ATP- and 2'-3'-O-(4-benzoylbenzoyl)-adenosine 5'-triphosphate (BzATP)-induced release of previously incorporated [3H]GABA. Both Brilliant Blue G and oxidized ATP inhibited the release of [3H]GABA caused by ATP application; the Brilliant Blue G-sensitive, P2X7 receptor-mediated fraction, was much larger after ischemia than after normoxia. Whereas ischemic stimulation failed to alter the amplitude of ATP- and BzATP-induced small inward currents recorded from a subset of non-pyramidal neurons, BzATP caused a more pronounced increase in the frequency of miniature inhibitory postsynaptic currents (mIPSCs) after ischemia than after normoxia. Brilliant Blue G almost abolished the effect of BzATP in normoxic neurons. Since neither the amplitude of mIPSCs nor that of the muscimol-induced inward currents was affected by BzATP, it is assumed that BzATP acts at presynaptic P2X7 receptors. Finally, P2X7 receptors did not enhance the intracellular free Ca2+ concentration either in proximal dendrites or in astrocytes, irrespective of the normoxic or ischemic pre-incubation conditions. Hence, facilitatory P2X7 receptors may be situated at the axon terminals of GABAergic non-pyramidal neurons. When compared with normoxia, ischemia appears to markedly increase P2X7 receptor-mediated GABA release, which may limit the severity of the ischemic damage. At the same time we did not find an accompanying enhancement of P2X7 mRNA or protein expression, suggesting that receptors may become hypersensitive because of an increased efficiency of their transduction pathways.

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  • P2X7R is detected in glial and neuronal cells.

    “Despite being detected in glial and neuronal cells [49,50,51,52,53,54], the activity of the P2X7R was not always investigated and used antibodies lack specificity [49,55,56,57].”

    From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [52]

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Authors
Wirkner, K., Köfalvi, A., Fischer, W., Günther, A., Franke, H., Gröger‐Arndt, H., Nörenberg, W., Madarász, E., Vizi, E. S., Schneider, D., Sperlágh, B., & Illes, P.
Affiliations
  • Leipzig University (DE)
  • HUN-REN Institute of Experimental Medicine (HU)
ORCID
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2005-09-12
Volume
95
Issue
5
Pages
1421-1437
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
DOI
10.1111/j.1471-4159.2005.03465.x
OpenAlex
W1574413143
Cited by
89
References
51
Citations by year
2026: 2 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 3 · 2020: 4 · 2019: 1 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 6 · 2014: 6 · 2013: 5 · 2012: 5
FWCI
3.84
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
Keywords
P2X7 receptor, receptor supersensitivity, cerebral ischemia, GABA release, GABAergic interneurons, BzATP, ATP, Brilliant Blue G, miniature inhibitory postsynaptic currents, intracellular calcium, astrocytes, serum deprivation, cortical neurons, excitotoxicity
MeSH terms
Adenosine Triphosphate, Anesthetics, Local, Animals, Bicuculline, Caffeine, Calcium, Cell Count, Cells, Cultured, Cerebral Cortex, Deoxyadenosines, Dose-Response Relationship, Drug, Drug Interactions, Electric Stimulation, Embryo, Mammalian, Enzyme Inhibitors, gamma-Aminobutyric Acid, Glial Fibrillary Acidic Protein, Immunohistochemistry, Ischemia, Membrane Potentials, Microtubule-Associated Proteins, Neurons, RNA, Messenger, Tetrodotoxin, Time Factors, Triazines, Tritium, Xanthines, 2-Amino-5-phosphonovalerate, Fura-2, Receptors, Purinergic P2, Patch-Clamp Techniques, Microscopy, Confocal, Excitatory Amino Acid Antagonists, 6-Cyano-7-nitroquinoxaline-2,3-dione, GABA Antagonists, Reverse Transcriptase Polymerase Chain Reaction, Rats, Receptors, Purinergic P2X7, In Vitro Techniques

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