Syntaxin 1A supports voltage-dependent inhibition of alpha(1B) Ca2+ channels by G beta gamma in chick sensory neurons

N-type Ca2+ channels are modulated by a variety of G-protein-coupled pathwa ys. Some pathways produce a transient, voltage-dependent (VD) inhibition of N channel function and involve direct binding of G-protein subunits; other s require the activation of intermediate enzymes and produce a longer-lasti ng, voltage-independent (VI) form of inhibition. The ratio of VD: VI inhibi tion differs significantly among cell types, suggesting that the two forms of inhibition play unique physiological roles in the nervous system. In thi s study, we explored mechanisms capable of altering the balance of VD and V I inhibition in chick dorsal root ganglion neurons. We report that (1) VD: VI inhibition is critically dependent on the G beta gamma concentration, wi th VI inhibition dominant at low G beta gamma concentrations, and (2) synta xin-1A (but not syntaxin-1B) shifts the ratio in favor of VD inhibition by potentiating the VD effects of G beta gamma. Variations in expression level s of G-proteins and/or syntaxin provide the means to alter over a wide rang e both the extent and the rate of Ca2+ influx through N channels.