QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, January 10, 2007, 27(2):265-269; doi:10.1523/JNEUROSCI.4213-06.2007

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Keith, R. K. Articles by Meriney, S. D. Search for Related Content PubMed PubMed Citation Articles by Keith, R. K. Articles by Meriney, S. D.

 Previous Article  |  Next Article 

Brief Communications
Bidirectional Modulation of Transmitter Release by Calcium Channel/Syntaxin Interactions In Vivo

Ryan K. Keith,¹ Robert E. Poage,¹ Charles T. Yokoyama,² William A. Catterall,² and Stephen D. Meriney¹

¹Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, and ²Department of Pharmacology and Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, Washington 98195-7280

Correspondence should be addressed to Stephen D. Meriney, Department of Neuroscience, 446 Crawford Hall, University of Pittsburgh, Pittsburgh, PA 15260. Email: meriney{at}bns.pitt.edu

Protein interactions within the active zone of the nerve terminal are critical for regulation of transmitter release. The SNARE protein syntaxin 1A, primarily known for important interactions that control vesicle fusion, also interacts with presynaptic voltage-gated calcium channels. Based on recordings of calcium channel function in vitro, it has been hypothesized that syntaxin 1A–calcium channel interactions could alter calcium channel function at synapses. However, results at synapses in vitro suggest two potentially opposing roles: enhancement of neurotransmitter release by positioning docked vesicles near calcium channels and inhibition of calcium channel function by interaction with SNARE proteins. We have examined the possibility that these two effects of syntaxin can occur at synapses by studying the effects on transmitter release of manipulating syntaxin 1A–calcium channel interactions at Xenopus tadpole tail neuromuscular synapses in vivo. Introduction of synprint peptides, which competitively perturb syntaxin 1A–calcium channel interactions, decreased quantal content at these synapses and increased paired-pulse and tetanic facilitation. In contrast, injecting mRNA for mutant (A240V, V244A) syntaxin 1A, which reduces calcium channel modulation but not binding in vitro, increased quantal content and decreased paired-pulse and tetanic facilitation. Injection of wild-type syntaxin 1A mRNA had no effect. The opposing effects of synprint peptides and mutant syntaxin 1A provide in vivo support for the hypothesis that these interactions serve both to colocalize calcium channels with the release machinery and to modulate the functional state of the calcium channel. As such, these two effects of syntaxin on calcium channels modulate transmitter release in a bidirectional manner.

Key words: calcium; syntaxin; synprint; neuromuscular junction; Xenopus; facilitation

---

Received April 13, 2006; revised Nov. 21, 2006; accepted Nov. 22, 2006.

Correspondence should be addressed to Stephen D. Meriney, Department of Neuroscience, 446 Crawford Hall, University of Pittsburgh, Pittsburgh, PA 15260. Email: meriney{at}bns.pitt.edu

This article has been cited by other articles:

				M. Zuzarte, K. Heusser, V. Renigunta, G. Schlichthorl, S. Rinne, E. Wischmeyer, J. Daut, B. Schwappach, and R. Preisig-Muller Intracellular traffic of the K+ channels TASK-1 and TASK-3: role of N- and C-terminal sorting signals and interaction with 14-3-3 proteins J. Physiol., March 1, 2009; 587(5): 929 - 952. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help