ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
ATP inhibits NMDA receptors after heterologous expression and in cultured hippocampal neurons and attenuates NMDA-mediated neurotoxicity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 36 citations in OpenAlex.
- Extracellular Adenosine Triphosphate Binding to P2Y1 Receptors Prevents Glutamate-Induced Excitotoxicity: Involvement of Erk1/2 Signaling Pathway to Suppress Autophagy.Frontiers in neuroscience · 2022Article
- Allosteric modulation of GABAA receptors by extracellular ATP.Molecular brain · 2014Article
- Intercellular signaling pathway among Endothelia, astrocytes and neurons in excitatory neuronal damage.International journal of molecular sciences · 2013Review
- Communication between corneal epithelial cells and trigeminal neurons is facilitated by purinergic (P2) and glutamatergic receptors.PloS one · 2012Article
- Tuning and fine-tuning of synapses with adenosine.Current neuropharmacology · 2009Article
- Factors affecting guanine nucleotide binding to rat AMPA receptors.Brain research · 2007Article
- Functions of neuronal P2Y receptors.Pflugers Archiv : European journal of physiology · 2006Review
- Voltage-dependent inhibition of recombinant NMDA receptor-mediated currents by 5-hydroxytryptamine.British journal of pharmacology · 2005Article
- Regulation of neuronal ion channels via P2Y receptors.Purinergic signalling · 2004Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the potential of ATP to inhibit heterologously expressed NMDA receptor subunit combinations, NMDA-induced currents in cultured hippocampal cells, and NMDA-induced neurotoxicity. The effect of ATP on diheteromeric NR1a/NR2A-D NMDA receptor (NR) combinations expressed in Xenopus laevis oocytes was studied by voltage-clamp recording. ATP strongly inhibited NMDA-induced inward currents only at the NR1a/NR2B receptor combination. At NMDA concentrations corresponding to the EC50 value (20 microm), ATP revealed an IC50 value of 135 microm. Mutation studies suggest that ATP exerts its inhibition via the glutamate-binding pocket of the NR2B subunit. Inosine 5'-triphosphate (ITP), GTP, and AMP also inhibited the recombinant NR1a/NR2B receptor, whereas UTP and CTP, ADP, or adenosine had no or only a small effect. Correspondingly, ATP inhibited NMDA-induced but not kainate-induced currents at cultured hippocampal neurons. An abundant expression of the NR2B subunit in the cultured neurons was verified by immunocytochemistry and blockade of NMDA-induced currents by the NR2B-selective antagonist ifenprodil. In addition we studied the role of ATP in NMDA-mediated neurotoxicity using cultured rat hippocampal cells. ATP exhibited a dose-dependent rescue effect when coapplied with the excitotoxicant NMDA, in contrast to ADP, AMP, and adenosine. The effect of ATP was mimicked by GTP and ITP but not by UTP and CTP. ATP had no effect on kainate-elicited neurotoxicity. Our results suggest that ATP can act as an inhibitor of NMDA receptors depending on receptor subunit composition and that it can attenuate NMDA-mediated neurotoxicity that is mediated neither by ATP nor by adenosine receptors.
Indexed as
Identifiers
12832522PMC6741184W2110092778What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.