ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
G-proteins modulate cumulative inactivation of N-type (Cav2.2) calcium channels.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- Article
- Molecular insights into the gating mechanisms of voltage-gated calcium channel CaNature communications · 2023Article
- Protofibrillar Amyloid Beta Modulation of Recombinant hCaV2.2 (N-Type) Voltage-Gated Channels.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Motor, epileptic, and developmental phenotypes in genetic disorders affecting G protein coupled receptors-cAMP signaling.Frontiers in neurology · 2022Review
- Emerging and converging molecular mechanisms in dystonia.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- Modulation of voltage-gated CaChannels (Austin, Tex.) · 2020Review
- Article
- Gβγ directly modulates vesicle fusion by competing with synaptotagmin for binding to neuronal SNARE proteins embedded in membranes.The Journal of biological chemistry · 2017Article
- Serotonin and Serotonin Transporters in the Adrenal Medulla: A Potential Hub for Modulation of the Sympathetic Stress Response.ACS chemical neuroscience · 2017Review
- Article
- Article
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- Gabapentin inhibits catecholamine release from adrenal chromaffin cells.Anesthesiology · 2012Article
- Up-regulation of Cavβ3 subunit in primary sensory neurons increases voltage-activated Ca2+ channel activity and nociceptive input in neuropathic pain.The Journal of biological chemistry · 2012Article
- Nitric oxide inhibits nociceptive transmission by differentially regulating glutamate and glycine release to spinal dorsal horn neurons.The Journal of biological chemistry · 2011Article
- Inhibition of Ca2+ channels and adrenal catecholamine release by G protein coupled receptors.Cellular and molecular neurobiology · 2010Review
- Voltage-dependent kappa-opioid modulation of action potential waveform-elicited calcium currents in neurohypophysial terminals.Journal of cellular physiology · 2010Article
- Scanning mutagenesis of the I-II loop of the Cav2.2 calcium channel identifies residues Arginine 376 and Valine 416 as molecular determinants of voltage dependent G protein inhibition.Molecular brain · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Precise regulation of N-type (Ca(V)2.2) voltage-gated calcium channels (Ca-channels) controls many cellular functions including neurotransmitter and hormone release. One important mechanism that inhibits Ca2+ entry involves binding of G-protein betagamma subunits (Gbetagamma) to the Ca-channels. This shifts the Ca-channels from "willing" to "reluctant" gating states and slows activation. Voltage-dependent reversal of the inhibition (facilitation) is thought to reflect transient dissociation of Gbetagamma from the Ca-channels and can occur during high-frequency bursts of action potential-like waveforms (APW). Inactivation of Ca-channels will also limit Ca2+ entry, but it remains unclear whether G-proteins can modulate inactivation. In part this is because of the complex nature of inactivation, and because facilitation of Ca-channel currents (I(Ca)) masks the extent and kinetics of inactivation during typical stimulation protocols. We used low-frequency trains of APW to activate I(Ca). This more closely mimics physiological stimuli and circumvents the problem of facilitation which does not occur at < or = 5 Hz. Activation of endogenous G-proteins reduced both Ca2+-dependent, and voltage-dependent inactivation of recombinant I(Ca) in human embryonic kidney 293 cells. This was mimicked by expression of wild-type Gbetagamma, but not by a point mutant of Gbetagamma with reduced affinity for Ca-channels. A similar decrease in the inactivation of I(Ca) was produced by P2Y receptors in adrenal chromaffin cells. Overall, our data identify and characterize a novel effect of G-proteins on I(Ca), and could have important implications for understanding how G-protein-coupled receptors control Ca2+ entry and Ca2+-dependent events such as neurotransmitter and hormone release.
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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.