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Syntaxin 1B is important for mouse postnatal survival and proper synaptic function at the mouse neuromuscular junctions

Item Type:Article
Title:Syntaxin 1B is important for mouse postnatal survival and proper synaptic function at the mouse neuromuscular junctions
Creators Name:Wu, Y.J. and Tejero, R. and Arancillo, M. and Vardar, G. and Korotkova, T. and Kintscher, M. and Schmitz, D. and Ponomarenko, A. and Tabares, L. and Rosenmund, C.
Abstract:STX1 is a major neuronal syntaxin protein located at the plasma membrane of the neuronal tissues. Rodent STX1 has two highly similar paralogs, STX1A and STX1B, that are thought to be functionally redundant. Interestingly, some studies have shown that the distribution patterns of STX1A and STX1B at the central and peripheral nervous systems only partially overlapped, implying that there might be differential functions between these paralogs. In the current study, we generated an STX1B knockout (KO) mouse line and studied the impact of STX1B removal in neurons of several brain regions and the neuromuscular junction (NMJ). We found that either complete removal of STX1B or selective removal of it from forebrain excitatory neurons in mice caused premature death. Autaptic hippocampal and striatal cultures derived from STX1B KO mice still maintained efficient neurotransmission compared with neurons from STX1B wild-type and heterozygous mice. Interestingly, examining high-density cerebellar cultures revealed a decrease in the spontaneous GABAergic transmission frequency, which was most likely due to a lower number of neurons in the STX1B KO cultures, suggesting that STX1B is essential for neuronal survival in vitro. Moreover, our study also demonstrated that although STX1B is dispensable for the formation of the mouse NMJ, it is required to maintain the efficiency of neurotransmission at the nerve-muscle synapse.
Keywords:SNARE, NMJ, Neurotransmitter Release, Spontaneous Release, Evoked Release, Animals, Mice
Source:Journal of Neurophysiology
ISSN:0022-3077
Publisher:American Physiological Society
Volume:114
Number:4
Page Range:2404-2417
Date:1 October 2015
Additional Information:Copyright © 2015 The American Physiological Society
Official Publication:https://doi.org/10.1152/jn.00577.2015
External Fulltext:View full text on PubMed Central
PubMed:View item in PubMed

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