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The Journal of Neuroscience, May 1, 2001, 21(9):2949-2957
Syntaxin 1A Supports Voltage-Dependent Inhibition of
 1B Ca2+ Channels by G  in Chick Sensory
Neurons
Qiang
Lü1,
M. S.
AtKisson1,
Scott E.
Jarvis2,
Zhong-Ping
Feng2, 3,
Gerald W.
Zamponi2, and
Kathleen
Dunlap1
1 Department of Neuroscience, Tufts University School
of Medicine, Boston, Massachusetts 02111, 2 Department of
Physiology and Biophysics, University of Calgary, Calgary, Alberta T2N
4N1, Canada, and 3 NeuroMed Technologies, Vancouver,
British Columbia V6T 1Z4, Canada
N-type Ca2+ channels are modulated by a variety
of G-protein-coupled pathways. Some pathways produce a transient,
voltage-dependent (VD) inhibition of N channel function and involve
direct binding of G-protein subunits; others require the activation of
intermediate enzymes and produce a longer-lasting, voltage-independent
(VI) form of inhibition. The ratio of VD:VI inhibition differs
significantly among cell types, suggesting that the two forms of
inhibition play unique physiological roles in the nervous system. In
this study, we explored mechanisms capable of altering the balance of
VD and VI inhibition in chick dorsal root ganglion neurons. We report
that (1) VD:VI inhibition is critically dependent on the G 
concentration, with VI inhibition dominant at low G concentrations, and (2) syntaxin-1A (but not syntaxin-1B) shifts the
ratio in favor of VD inhibition by potentiating the VD effects of
G. Variations in expression levels of G-proteins and/or syntaxin provide the means to alter over a wide range both the extent and the
rate of Ca2+ influx through N channels.
Key words:
G-protein modulation; dorsal root ganglion neurons; GABA
receptors; adrenergic receptors; recombinant channels; presynaptic
regulation
Copyright © 2001 Society for Neuroscience 0270-6474/01/2192949-09$05.00/0
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