ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
The Ca2+ channel beta3 subunit differentially modulates G-protein sensitivity of alpha1A and alpha1B Ca2+ channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Structure and function of the β subunit of voltage-gated Ca²⁺ channels.Biochimica et biophysica acta · 2013Review
- The ß subunit of voltage-gated Ca2+ channels.Physiological reviews · 2010Review
- Stargazin modulates neuronal voltage-dependent Ca(2+) channel Ca(v)2.2 by a Gbetagamma-dependent mechanism.The Journal of biological chemistry · 2010Article
- Intracellular Na+ inhibits voltage-dependent N-type Ca2+ channels by a G protein betagamma subunit-dependent mechanism.The Journal of physiology · 2004Article
- Enhanced G protein-dependent modulation of excitatory synaptic transmission in the cerebellum of the Ca2+ channel-mutant mouse, tottering.The Journal of physiology · 2003Article
- Mutations in high-voltage-activated calcium channel genes stimulate low-voltage-activated currents in mouse thalamic relay neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Differential facilitation of N- and P/Q-type calcium channels during trains of action potential-like waveforms.The Journal of physiology · 2002Article
- Protein kinase C is involved in M1-muscarinic receptor-mediated facilitation of L-type Ca2+ channels in neurons of the major pelvic ganglion of the adult male rat.Neurochemical research · 2001Article
- Syntaxin 1A supports voltage-dependent inhibition of alpha1B Ca2+ channels by Gbetagamma in chick sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- G-protein inhibition of N- and P/Q-type calcium channels: distinctive elementary mechanisms and their functional impact.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Interaction between G proteins and accessory subunits in the regulation of 1B calcium channels in Xenopus oocytes.The Journal of physiology · 2000Article
- Calcium channel beta subunit promotes voltage-dependent modulation of alpha 1 B by G beta gamma.Biophysical journal · 2000Article
- Differential occurrence of reluctant openings in G-protein-inhibited N- and P/Q-type calcium channels.The Journal of general physiology · 2000Article
- delta opioid receptor modulation of several voltage-dependent Ca(2+) currents in rat sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Targeted disruption of the Ca2+ channel beta3 subunit reduces N- and L-type Ca2+ channel activity and alters the voltage-dependent activation of P/Q-type Ca2+ channels in neurons.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Ca2+ channel beta3 subunit enhances voltage-dependent relief of G-protein inhibition induced by muscarinic receptor activation and Gbetagamma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Identification of the amino terminus of neuronal Ca2+ channel alpha1 subunits alpha1B and alpha1E as an essential determinant of G-protein modulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We have shown previously that the Ca2+ channel beta3 subunit is capable of modulating tonic G-protein inhibition of alpha1A and alpha1B Ca2+ channels expressed in oocytes. Here we determine the modulatory effect of the Ca2+ channel beta3 subunit on M2 muscarinic receptor-activated G-protein inhibition and whether the beta3 subunit modulates the G-protein sensitivity of alpha1A and alpha1B currents equivalently. To compare the relative inhibition by muscarinic activation, we have used successive ACh applications to remove the large tonic inhibition of these channels. We show that the resulting rebound potentiation results entirely from the loss of tonic G-protein inhibition; although the currents are temporarily relieved of tonic inhibition, they are still capable of undergoing inhibition through the muscarinic pathway. Using this rebound protocol, we demonstrate that the inhibition of peak current amplitude produced by M2 receptor activation is similar for alpha1A and alpha1B calcium currents. However, the contribution of the voltage-dependent component of inhibition, characterized by reduced inhibition at very depolarized voltage steps and the relief of inhibition by depolarizing prepulses, was slightly greater for the alpha1B current than for the alpha1A current. After co-expression of the beta3 subunit, the sensitivity to M2 receptor-induced G-protein inhibition was reduced for both alpha1A and alpha1B currents; however, the reduction was significantly greater for alpha1A currents. Additionally, the difference in the voltage dependence of inhibition of alpha1A and alpha1B currents was heightened after co-expression of the Ca2+ channel beta3 subunit. Such differential modulation of sensitivity to G-protein modulation may be important for fine tuning release in neurons that contain both of these Ca2+ channels.
Indexed as
Identifiers
9437009PMC6792773W1608854978What OpenQuestion holds
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.