ArticleMolecular and cellular neurosciences2010
Conantokins inhibit NMDAR-dependent calcium influx in developing rat hippocampal neurons in primary culture with resulting effects on CREB phosphorylation.
Article in Molecular and cellular neurosciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Antagonistic action on NMDA/GluN2B mediated currents of two peptides that were conantokin-G structure-based designed.BMC neuroscience · 2017Article
- Pharmacology of triheteromeric N-Methyl-D-Aspartate Receptors.Neuroscience letters · 2016Article
- Hydroxyproline-induced Helical Disruption in Conantokin Rl-B Affects Subunit-selective Antagonistic Activities toward Ion Channels of N-Methyl-d-aspartate Receptors.The Journal of biological chemistry · 2015Article
- Probing NMDA receptor GluN2A and GluN2B subunit expression and distribution in cortical neurons.Neuropharmacology · 2014Article
- Roles of phosphotase 2A in nociceptive signal processing.Molecular pain · 2013Review
- Antagonist properties of Conus parius peptides on N-methyl-D-aspartate receptors and their effects on CREB signaling.PloS one · 2013Article
- Opposing action of conantokin-G on synaptically and extrasynaptically-activated NMDA receptors.Neuropharmacology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The effects of conantokin (con)-G, con-R[1-17], and con-T on ion flow through N-methyl-D-aspartate receptor (NMDAR) ion channels were determined in cultured primary rat hippocampal neurons. The potency of con-G diminished, whereas inhibition by con-R[1-17] and con-T did not change, as the neurons matured. Con-G, con-R[1-17], and con-T effectively diminished NMDA-induced Ca(2+) influx into the cells. A similar age-dependent decrease in con-G-mediated inhibition of the amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) was observed, compared to con-R[1-17] and con-T. The effects of the conantokins on NMDA-induced cAMP response element-binding protein (CREB) phosphorylation in immature (DIV 9) and mature (DIV 16) neurons showed that, at DIV 9, con-G, con-R[1-17], and con-T inhibited NMDA-mediated P-CREB levels, whereas in DIV 16 neurons the conantokins did not inhibit overall levels of NMDA-induced P-CREB. In contrast, P-CREB levels were enhanced through inhibition of the protein phosphatases, PP1 and PP2B (calcineurin). This ability of conantokins to sustain CREB phosphorylation can thus enhance neuronal survival and plasticity.
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