Calcium Channel β Subunit Promotes Voltage-Dependent Modulation of α1B by Gβγ
By A. Meir, D. Bell, G. Stephens, K. Page, A. Dolphin. 2000
94 citations recorded by the source corpus.
Abstract Voltage-dependent calcium channels (VDCCs) are heteromultimers composed of a pore-forming α 1 subunit and auxiliary subunits, including the intracellular β subunit, which has a strong influence on the channel properties. Voltage-dependent inhibitory modulation of neuronal VDCCs occurs primarily by activation of G-proteins and elevation of the free G βγ dimer concentration. Here we have examined the interaction between the regulation of N-type ( α 1B) channels by their β subunits and by G βγ dimers, heterologously expressed in COS-7 cells. In contrast to previous studies suggesting antagonism of G protein inhibition by the VDCC β subunit, we found a significantly larger G βγ -dependent inhibition of α 1B channel activation when the VDCC α 1B and β subunits were coexpressed. In the absence of coexpressed VDCC β subunit, the G βγ dimers, either expressed tonically or elevated via receptor activation, did not produce the expected features of voltage-dependent G protein modulation of N-type channels, including slowed activation and prepulse facilitation, while VDCC β subunit coexpression restored all of the hallmarks of G βγ modulation. These results suggest that the VDCC β subunit must be present for G βγ to induce voltage-dependent modulation of N-type calcium channels.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/5306c0ec8048cb4ed88cf0158a3aeea3b35886f1
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In Cellular and Molecular Neuroscience
In Molecular Biology
Citations in the corpus
- Ca2+ channel β-subunits: structural insights AID our understanding (2004, unknown): “Gbg binding at depolarized potentials and induces their removal, resulting in prepulse potentiation [14, 36 ].”
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential (2015, background): “All of the CaVb subunits increase the maximum single channel open probability, which will increase current through individual channels, and will thus result in increased macroscopic current density (Matsuyama et al., 1999; Meir et al., 2000; Neely et al., 2004).”
- Evidence for Two Concentration-Dependent Processes for β-Subunit Effects on α1B Calcium Channels (2001, unknown): “In a previous study in COS-7 cells, we found that tonic voltage-dependent G protein modulation via co-expressed G␥ dimers (as detected by its reversal by a depolarizing prepulse) was lost in the absence of coexpressed -subunit (Meir et al., 2000).”