Journal
NATURE NEUROSCIENCE
Volume 13, Issue 3, Pages 338-U16Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2488
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Funding
- National Cancer Institute Intramural Research Program
- National Institute of Neurological Disorders and Stroke Intramural Research Program
- Integrative Neural Immune Program
- National Institute on Deafness and other Communication Disorders
- NATIONAL CANCER INSTITUTE [ZIABC011035, ZIABC009404] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [ZIANS003035, ZIANS002994] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS [ZIADC000003] Funding Source: NIH RePORTER
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Regulated exocytosis is essential for many biological processes and many components of the protein trafficking machinery are ubiquitous. However, there are also exceptions, such as SNAP-25, a neuron-specific SNARE protein that is essential for synaptic vesicle release from presynaptic nerve terminals. In contrast, SNAP-23 is a ubiquitously expressed SNAP-25 homolog that is critical for regulated exocytosis in non-neuronal cells. However, the role of SNAP-23 in neurons has not been elucidated. We found that SNAP-23 was enriched in dendritic spines and colocalized with constituents of the postsynaptic density, whereas SNAP-25 was restricted to axons. In addition, loss of SNAP-23 using genetically altered mice or shRNA targeted to SNAP-23 led to a marked decrease in NMDA receptor surface expression and NMDA receptor currents, whereas loss of SNAP-25 did not. SNAP-23 is therefore important for the functional regulation of postsynaptic glutamate receptors.
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