• Takumi Fujita, Michael J Chen, Baoman Li, Nathan A Smith, Weiguo Peng, Wei Sun, Michael J Toner, Benjamin T Kress, Linhui Wang, Abdellatif Benraiss, Takahiro Takano, Su Wang, and Maiken Nedergaard.
• Center for Translational Neuromedicine, University of Rochester Medical School, Rochester, New York 14642 nedergaard@urmc.rochester.edu Takumi_Fujita@urmc.rochester.edu.
• J. Neurosci. 2014 Dec 10;34(50):16594-604.

AbstractExperimental advances in the study of neuroglia signaling have been greatly accelerated by the generation of transgenic mouse models. In particular, an elegant manipulation that interferes with astrocyte vesicular release of gliotransmitters via overexpression of a dominant-negative domain of vesicular SNARE (dnSNARE) has led to documented astrocytic involvement in processes that were traditionally considered strictly neuronal, including the sleep-wake cycle, LTP, cognition, cortical slow waves, depression, and pain. A key premise leading to these conclusions was that expression of the dnSNARE was specific to astrocytes. Inconsistent with this premise, we report here widespread expression of the dnSNARE transgene in cortical neurons. We further demonstrate that the activity of cortical neurons is reversibly suppressed in dnSNARE mice. These findings highlight the need for independent validation of astrocytic functions identified in dnSNARE mice and thus question critical evidence that astrocytes contribute to neurotransmission through SNARE-dependent vesicular release of gliotransmitters.Copyright © 2014 the authors 0270-6474/14/3416594-11$15.00/0.

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