Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
J Physiol
2004 Oct 15;560Pt 2:351-63. doi: 10.1113/jphysiol.2004.068817.
Show Gene links
Show Anatomy links
Syntaxin 1A regulation of weakly inactivating N-type Ca2+ channels.
Hurley JH
,
Cahill AL
,
Wang M
,
Fox AP
.
???displayArticle.abstract???
N- and P/Q-type Ca2+ channels are abundant in nerve terminals where they interact with proteins of the release apparatus, including syntaxin 1A and SNAP-25. In previous studies on N- or P/Q-type Ca2+ channels, syntaxin 1A co-expression reduced current amplitudes, increased voltage-dependent inactivation and/or enhanced G-protein inhibition. However, these studies were conducted in Ca2+ channels that exhibited significant voltage-dependent inactivation. We previously reported that N-type current in bovine chromaffin cells exhibits very little voltage-dependent inactivation and we identified the Ca2+ channel subunits involved. This study was undertaken to determine the effect of syntaxin 1A on this weakly inactivating Ca2+ channel. Co-expression of syntaxin 1A with the weakly inactivating bovine N-type Ca2+ channels in Xenopus oocytes did not appear to alter inactivation but dramatically reduced current amplitudes, without changing cell surface expression. To further understand the mechanisms of syntaxin 1A regulation of this weakly inactivating channel, we examined mutants of the alpha1B subunit, beta2a subunit and syntaxin 1A. We determined that the synprint site of alpha1B and the C-terminal third of syntaxin 1A were necessary for the reduced current amplitude. In addition we show that enhanced G-protein-dependent modulation of the Ca2+ current by syntaxin 1A cannot explain the large suppression of Ca2+ current observed. Of most significance, syntaxin 1A increased voltage-dependent inactivation in channels containing mutant beta2a subunits that cannot be palmitoylated. Our data suggest that changes in inactivation can not explain the reduction in current amplitude produced by co-expressing syntaxin and a weakly inactivating Ca2+ channel.
Artalejo,
Omega-conotoxin GVIA blocks a Ca2+ current in bovine chromaffin cells that is not of the "classic" N type.
1992, Pubmed
Artalejo,
Omega-conotoxin GVIA blocks a Ca2+ current in bovine chromaffin cells that is not of the "classic" N type.
1992,
Pubmed
Bennett,
Syntaxin: a synaptic protein implicated in docking of synaptic vesicles at presynaptic active zones.
1992,
Pubmed
Bezprozvanny,
Functional impact of syntaxin on gating of N-type and Q-type calcium channels.
1995,
Pubmed
,
Xenbase
Bezprozvanny,
Molecular determinants of the functional interaction between syntaxin and N-type Ca2+ channel gating.
2000,
Pubmed
,
Xenbase
Bourinet,
Determinants of the G protein-dependent opioid modulation of neuronal calcium channels.
1996,
Pubmed
,
Xenbase
Cahill,
Coexpression of cloned alpha(1B), beta(2a), and alpha(2)/delta subunits produces non-inactivating calcium currents similar to those found in bovine chromaffin cells.
2000,
Pubmed
,
Xenbase
Cox,
Inactivation of N-type calcium current in chick sensory neurons: calcium and voltage dependence.
1994,
Pubmed
Degtiar,
Syntaxin modulation of slow inactivation of N-type calcium channels.
2000,
Pubmed
,
Xenbase
Dolphin,
Mechanisms of modulation of voltage-dependent calcium channels by G proteins.
1998,
Pubmed
Ellinor,
Functional expression of a rapidly inactivating neuronal calcium channel.
1993,
Pubmed
,
Xenbase
Feng,
Calcium channel beta subunits differentially regulate the inhibition of N-type channels by individual Gbeta isoforms.
2001,
Pubmed
Hering,
Molecular determinants of inactivation in voltage-gated Ca2+ channels.
2000,
Pubmed
Hirning,
Dominant role of N-type Ca2+ channels in evoked release of norepinephrine from sympathetic neurons.
1988,
Pubmed
Horne,
The effect of omega-conotoxin GVIA on synaptic transmission within the nucleus accumbens and hippocampus of the rat in vitro.
1991,
Pubmed
Horton,
Syntaxin 1A up-regulates GABA transporter expression by subcellular redistribution.
2001,
Pubmed
,
Xenbase
Horton,
Engineering hybrid genes without the use of restriction enzymes: gene splicing by overlap extension.
1989,
Pubmed
Hurley,
The role of dynamic palmitoylation in Ca2+ channel inactivation.
2000,
Pubmed
Jarvis,
G protein modulation of N-type calcium channels is facilitated by physical interactions between syntaxin 1A and Gbetagamma.
2000,
Pubmed
Jarvis,
Distinct molecular determinants govern syntaxin 1A-mediated inactivation and G-protein inhibition of N-type calcium channels.
2001,
Pubmed
Jarvis,
Molecular determinants of syntaxin 1 modulation of N-type calcium channels.
2002,
Pubmed
Liang,
Unified mechanisms of Ca2+ regulation across the Ca2+ channel family.
2003,
Pubmed
Luebke,
Multiple calcium channel types control glutamatergic synaptic transmission in the hippocampus.
1993,
Pubmed
Lévêque,
Purification of the N-type calcium channel associated with syntaxin and synaptotagmin. A complex implicated in synaptic vesicle exocytosis.
1994,
Pubmed
Lü,
Syntaxin 1A supports voltage-dependent inhibition of alpha1B Ca2+ channels by Gbetagamma in chick sensory neurons.
2001,
Pubmed
Masaki,
Important roles of the C-terminal portion of HPC-1/syntaxin 1A in membrane anchoring and intracellular localization.
1998,
Pubmed
Michaelevski,
Direct interaction of target SNAREs with the Kv2.1 channel. Modal regulation of channel activation and inactivation gating.
2003,
Pubmed
,
Xenbase
Missler,
The making of neurexins.
1998,
Pubmed
Missler,
Alpha-neurexins couple Ca2+ channels to synaptic vesicle exocytosis.
2003,
Pubmed
Olcese,
The amino terminus of a calcium channel beta subunit sets rates of channel inactivation independently of the subunit's effect on activation.
1994,
Pubmed
,
Xenbase
Peters,
Syntaxin 1A inhibits regulated CFTR trafficking in xenopus oocytes.
1999,
Pubmed
,
Xenbase
Qin,
Unique regulatory properties of the type 2a Ca2+ channel beta subunit caused by palmitoylation.
1998,
Pubmed
,
Xenbase
Restituito,
The [beta]2a subunit is a molecular groom for the Ca2+ channel inactivation gate.
2000,
Pubmed
,
Xenbase
Rettig,
Isoform-specific interaction of the alpha1A subunits of brain Ca2+ channels with the presynaptic proteins syntaxin and SNAP-25.
1996,
Pubmed
Sheng,
Identification of a syntaxin-binding site on N-type calcium channels.
1994,
Pubmed
Spafford,
Expression and modulation of an invertebrate presynaptic calcium channel alpha1 subunit homolog.
2003,
Pubmed
Stanley,
Cleavage of syntaxin prevents G-protein regulation of presynaptic calcium channels.
1997,
Pubmed
Stanley,
Syntaxin I modulation of presynaptic calcium channel inactivation revealed by botulinum toxin C1.
2003,
Pubmed
Stanley,
Characterization of a calcium current in a vertebrate cholinergic presynaptic nerve terminal.
1991,
Pubmed
Takahashi,
Different types of calcium channels mediate central synaptic transmission.
1993,
Pubmed
Trus,
The transmembrane domain of syntaxin 1A negatively regulates voltage-sensitive Ca(2+) channels.
2001,
Pubmed
,
Xenbase
Turner,
Multiple Ca2+ channel types coexist to regulate synaptosomal neurotransmitter release.
1993,
Pubmed
Wheeler,
Roles of N-type and Q-type Ca2+ channels in supporting hippocampal synaptic transmission.
1994,
Pubmed
Williams,
Structure and functional expression of an omega-conotoxin-sensitive human N-type calcium channel.
1992,
Pubmed
Wiser,
Functional interaction of syntaxin and SNAP-25 with voltage-sensitive L- and N-type Ca2+ channels.
1996,
Pubmed
,
Xenbase
Wiser,
The voltage sensitive Lc-type Ca2+ channel is functionally coupled to the exocytotic machinery.
1999,
Pubmed
,
Xenbase
Zamponi,
Modulation of voltage-dependent calcium channels by G proteins.
1998,
Pubmed
