ArticlePloS one2011
Cyclic ADP ribose-dependent Ca2+ release by group I metabotropic glutamate receptors in acutely dissociated rat hippocampal neurons.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 10 citations in OpenAlex.
- mGluR5-dependent modulation of dendritic excitability in CA1 pyramidal neurons mediated by enhancement of persistent NaThe Journal of physiology · 2018Article
- Costimulation of AMPA and metabotropic glutamate receptors underlies phospholipase C activation by glutamate in hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Studies on the effect of adenosine on calcium oscillation in hippocampal neurons.Experimental and therapeutic medicine · 2013Article
- Group I mGluR-mediated inhibition of Kir channels contributes to retinal Müller cell gliosis in a rat chronic ocular hypertension model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group I metabotropic glutamate receptors (group I mGluRs; mGluR1 and mGluR5) exert diverse effects on neuronal and synaptic functions, many of which are regulated by intracellular Ca(2+). In this study, we characterized the cellular mechanisms underlying Ca(2+) mobilization induced by (RS)-3,5-dihydroxyphenylglycine (DHPG; a specific group I mGluR agonist) in the somata of acutely dissociated rat hippocampal neurons using microfluorometry. We found that DHPG activates mGluR5 to mobilize intracellular Ca(2+) from ryanodine-sensitive stores via cyclic adenosine diphosphate ribose (cADPR), while the PLC/IP(3) signaling pathway was not involved in Ca(2+) mobilization. The application of glutamate, which depolarized the membrane potential by 28.5±4.9 mV (n = 4), led to transient Ca(2+) mobilization by mGluR5 and Ca(2+) influx through L-type Ca(2+) channels. We found no evidence that mGluR5-mediated Ca(2+) release and Ca(2+) influx through L-type Ca(2+) channels interact to generate supralinear Ca(2+) transients. Our study provides novel insights into the mechanisms of intracellular Ca(2+) mobilization by mGluR5 in the somata of hippocampal neurons.
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