Determinants of G Protein Inhibition of Presynaptic Calcium Channels

2001 ◽  
Vol 34 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Gerald W. Zamponi
Keyword(s):  
Calcium Channels ◽  
G Protein ◽  
Protein Inhibition ◽  
Presynaptic Calcium

Cleavage of syntaxin prevents G-protein regulation of presynaptic calcium channels

Nature ◽  
1997 ◽  
Vol 385 (6614) ◽  
pp. 340-343 ◽  
Author(s):  
E. F. Stanley ◽  
R. R. Mirotznik
Keyword(s):  
Calcium Channels ◽  
G Protein ◽  
Protein Regulation ◽  
Presynaptic Calcium

scholarly journals Regulators of G Protein Signaling Proteins as Determinants of the Rate of Desensitization of Presynaptic Calcium Channels

1999 ◽  
Vol 274 (20) ◽  
pp. 14490-14494 ◽  
Author(s):  
Marı́a A. Diversé-Pierluissi ◽  
Thierry Fischer ◽  
J. Dedrick Jordan ◽  
Max Schiff ◽  
Daniel F. Ortiz ◽  
...  
Keyword(s):  
Calcium Channels ◽  
G Protein ◽  
G Protein Signaling ◽  
Signaling Proteins ◽  
Protein Signaling ◽  
Presynaptic Calcium

scholarly journals Differential Occurrence of Reluctant Openings in G-Protein–Inhibited N- and P/Q-Type Calcium Channels

2000 ◽  
Vol 115 (2) ◽  
pp. 175-192 ◽  
Author(s):  
Henry M. Colecraft ◽  
Parag G. Patil ◽  
David T. Yue
Keyword(s):  
Calcium Channels ◽  
G Protein ◽  
Action Potentials ◽  
Qualitative Difference ◽  
Hek 293 ◽  
Protein Inhibition ◽  
Voltage Dependent ◽  
Dependent Inhibition ◽  
Time Courses ◽  
Prepulse Facilitation

Voltage-dependent inhibition of N- and P/Q-type calcium channels by G proteins is crucial for presynaptic inhibition of neurotransmitter release, and may contribute importantly to short-term synaptic plasticity. Such calcium-channel modulation could thereby impact significantly the neuro-computational repertoire of neural networks. The differential modulation of N and P/Q channels could even further enrich their impact upon synaptic tuning. Here, we performed in-depth comparison of the G-protein inhibition of recombinant N and P/Q channels, expressed in HEK 293 cells with the m2 muscarinic receptor. While both channel types display classic features of G-protein modulation (kinetic slowing of activation, prepulse facilitation, and voltage dependence of inhibition), we confirmed previously reported quantitative differences, with N channels displaying stronger inhibition and greater relief of inhibition by prepulses. A more fundamental, qualitative difference in the modulation of these two channels was revealed by a modified tail-activation paradigm, as well as by a novel “slope” analysis method comparing time courses of slow activation and prepulse facilitation. The stark contrast in modulatory behavior can be understood within the context of the “willing–reluctant” model, in which binding of G-protein βγ subunits to channels induces a reluctant mode of gating, where stronger depolarization is required for opening. Our experiments suggest that only N channels could be opened in the reluctant mode, at voltages normally spanned by neuronal action potentials. By contrast, P/Q channels appear to remain closed, especially over these physiological voltages. Further, the differential occurrence of reluctant openings is not explained by differences in the rate of G-protein unbinding from the two channels. These two scenarios predict very different effects of G-protein inhibition on the waveform of Ca2+ entry during action potentials, with potentially important consequences for the timing and efficacy of synaptic transmission.

scholarly journals G protein inhibition of CaV2 calcium channels

Channels ◽  
2010 ◽  
Vol 4 (6) ◽  
pp. 497-509 ◽  
Author(s):  
Kevin P.M. Currie
Keyword(s):  
Calcium Channels ◽  
G Protein ◽  
Protein Inhibition

Abolition of G protein inhibition of α 1A and α 1B calcium channels by co-expression of the β 3 subunit

FEBS Letters ◽  
1995 ◽  
Vol 371 (1) ◽  
pp. 43-46 ◽  
Author(s):  
John P. Roche ◽  
Vellareddy Anantharam ◽  
Steven N. Treistman
Keyword(s):  
Calcium Channels ◽  
G Protein ◽  
Protein Inhibition
Sign in / Sign up

Export Citation Format

Share Document