ArticleThe Journal of physiology2010
Glutamate-induced internalization of Ca(v)1.3 L-type Ca(2+) channels protects retinal neurons against excitotoxicity.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Mechanisms controlling the trafficking, localization, and abundance of presynaptic CaFrontiers in molecular neuroscience · 2022Review
- Regulation of the parental gene GRM4 by circGrm4 RNA transcript and glutamate-mediated neurovascular toxicity in eyes.Molecular and cellular biochemistry · 2021Review
- Gamma oscillations in the pedunculopontine nucleus are regulated by F-actin: neuroepigenetic implications.American journal of physiology. Cell physiology · 2020Article
- Circadian regulation in the retina: From molecules to network.The European journal of neuroscience · 2020Review
- Possible Pharmacodynamic Interaction of Azelnidipine with Citicoline Against Ischemic Brain Injury: Behavioral, Biochemical and Histological Alterations.Annals of neurosciences · 2020Article
- Mouse retinal ganglion cell signalling is dynamically modulated through parallel anterograde activation of cannabinoid and vanilloid pathways.The Journal of physiology · 2017Article
- α-Actinin Promotes Surface Localization and Current Density of the CaBiochemistry · 2017Article
- Calcium dynamics and regulation in horizontal cells of the vertebrate retina: lessons from teleosts.Journal of neurophysiology · 2017Review
- The Contribution of L-Type CaFrontiers in molecular neuroscience · 2017Article
- Article
- The role of glutamate in neuronal ischemic injury: the role of spark in fire.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2012Review
- Different subcellular populations of L-type Ca2+ channels exhibit unique regulation and functional roles in cardiomyocytes.Journal of molecular and cellular cardiology · 2012Review
- Trafficking of presynaptic PMCA signaling complexes in mouse photoreceptors requires Cav1.4 α1 subunits.Advances in experimental medicine and biology · 2012Article
- The dynamic architecture of photoreceptor ribbon synapses: cytoskeletal, extracellular matrix, and intramembrane proteins.Visual neuroscience · 2011Review
- Cav1.4 IT mouse as model for vision impairment in human congenital stationary night blindness type 2.Channels (Austin, Tex.)Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Glutamate-induced rise in the intracellular Ca(2+) level is thought to be a major cause of excitotoxic cell death, but the mechanisms that control the Ca(2+) overload are poorly understood. Using immunocytochemistry, electrophysiology and Ca(2+) imaging, we show that activation of ionotropic glutamate receptors induces a selective internalization of Ca(v)1.3 L-type Ca(2+) channels in salamander retinal neurons. The effect of glutamate on Ca(v)1.3 internalization was blocked in Ca(2+)-free external solution, or by strong buffering of internal Ca(2+) with BAPTA. Downregulation of L-type Ca(2+) channel activity in retinal ganglion cells by glutamate was suppressed by inhibitors of dynamin-dependent endocytosis. Stabilization of F-actin by jasplakinolide significantly reduced the ability of glutamate to induce internalization suggesting it is mediated by Ca(2+)-dependent reorganization of actin cytoskeleton. We showed that the Ca(v)1.3 is the primary L-type Ca(2+) channel contributing to kainate-induced excitotoxic death of amacrine and ganglion cells. Block of Ca(v)1.3 internalization by either dynamin inhibition or F-actin stabilization increased vulnerability of retinal amacrine and ganglion cells to kainate-induced excitotoxicity. Our data show for the first time that Ca(v)1.3 L-type Ca(2+) channels are subject to rapid glutamate-induced internalization, which may serve as a negative feedback mechanism protecting retinal neurons against glutamate-induced excitotoxicity.
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