ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Insulin-like growth factor-1 modulation of CaV1.3 calcium channels depends on Ca2+ release from IP3-sensitive stores and calcium/calmodulin kinase II phosphorylation of the alpha1 subunit EF hand.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed, 65 citations in OpenAlex.
- PRMT5-Cacna1d axis maintains calcium homeostasis to regulate postnatal motor development in mice.Cellular and molecular life sciences : CMLS · 2026Article
- Mitochondrial Glutamine Metabolism Drives Epileptogenesis in Primary Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Mechanism of gabapentinoid potentiation of opioid effects on cyclic AMP signaling in neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Role of Insulin-like Growth Factor-1 Receptor in Tobacco Smoking-Associated Lung Cancer Development.Biomedicines · 2024Review
- The neurobiology of insulin-like growth factor I: From neuroprotection to modulation of brain states.Molecular psychiatry · 2023Review
- Identification of the molecular mechanism of insulin-like growth factor-1 (IGF-1): a promising therapeutic target for neurodegenerative diseases associated with metabolic syndrome.Cell & bioscience · 2023Review
- Pathophysiology of CaFrontiers in physiology · 2023Review
- Cytosolic peptides encoding CaCommunications biology · 2022Article
- Review
- Neuronal L-Type Calcium Channel Signaling to the Nucleus Requires a Novel CaMKIIα-Shank3 Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Amyloid-Beta Modulates Low-Threshold Activated Voltage-Gated L-Type Calcium Channels of Arcuate Neuropeptide Y Neurons Leading to Calcium Dysregulation and Hypothalamic Dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Dopamine neuron-derived IGF-1 controls dopamine neuron firing, skill learning, and exploration.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The Paroxysmal Depolarization Shift: Reconsidering Its Role in Epilepsy, Epileptogenesis and Beyond.International journal of molecular sciences · 2019Review
- Improved calcium sensor GCaMP-X overcomes the calcium channel perturbations induced by the calmodulin in GCaMP.Nature communications · 2018Article
- Splice variants of the CaScientific reports · 2016Article
- Protein kinase A modulation of CaV1.4 calcium channels.Nature communications · 2016Article
- Ca(2+) entry into neurons is facilitated by cooperative gating of clustered CaV1.3 channels.eLife · 2016Article
- Does Increased IGF-1 Concentration Have a Clear Positive Significance in Reducing Depression and Posttraumatic Arousal Symptoms?Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2015Article
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.Pharmacological reviews · 2015Review
- Differential CaMKII regulation by voltage-gated calcium channels in the striatum.Molecular and cellular neurosciences · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In neurons, L-type calcium channels (CaV1.2 and CaV1.3) regulate an extensive range of functions. However, the roles of CaV1.3-containing L channels, which are physiologically and pharmacologically distinct from the better understood CaV1.2 channels, are only beginning to be determined. We find that CaV1.3 channels are modulated by the insulin-like growth factor-1/receptor tyrosine kinase (IGF-1/RTK) through a signaling pathway that involves phospholipase C, calcium release from IP3-sensitive internal stores, and calcium/calmodulin kinase II. In addition, we find that the IGF-1-induced modulation requires phosphorylation of a specific serine residue, S1486, in the EF hand motif of the CaV1.3 subunit. This modulation alters CaV1.3 activity, causing a left shift in the current-voltage relationship and strongly potentiating peak currents at hyperpolarized membrane potentials. We also find that CaV1.3 channels and their RTK-dependent potentiation contribute to the regulation of the survival-promoting transcription factor cAMP response element-binding protein (CREB): in both cortical and hippocampal neurons, depolarization and IGF-1 rapidly increase phospho-CREB levels in a manner that requires CaV1.3 activity and the S1486 phosphorylation site to achieve a full effect. Although the full effects of CaV1.3 channels remain to be determined, their preferential localization to dendritic shafts and spine heads coupled with their ability to activate at relatively hyperpolarized and even subthreshold potentials suggests that CaV1.3 activity may subserve different cellular functions from CaV1.2 and, in particular, may be important in transducing signals initiated by excitatory neurotransmission.
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Registered trials
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