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Cell-specific loss of SNAP25 from cortical projection neurons allows normal development but causes subsequent neurodegeneration

Abstract:

Synaptosomal associated protein 25 kDa (SNAP25) is an essential component of the SNARE complex regulating synaptic vesicle fusion. SNAP25 deficiency has been implicated in a variety of cognitive disorders. We ablated SNAP25 from selected neuronal populations by generating a transgenic mouse (B6-Snap25tm3mcw (Snap25-flox)) with LoxP sites flanking exon5a/ 5b. In the presence of Cre-recombinase, Snap25-flox is recombined to a truncated transcript. Evoked synaptic vesicle release is severely red...

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Publication status:
Published
Peer review status:
Peer reviewed
Version:
Accepted Manuscript

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Publisher copy:
10.1093/cercor/bhy127

Authors


More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
Physiology Anatomy and Genetics
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
Physiology Anatomy and Genetics
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
Physiology Anatomy and Genetics
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
Pharmacology
Ramirez, DMO More by this author
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Publisher:
Oxford University Press Publisher's website
Journal:
Cerebral Cortex Journal website
Publication date:
2018-05-30
Acceptance date:
2018-05-05
DOI:
EISSN:
1460-2199
ISSN:
1047-3211
Pubs id:
pubs:854566
URN:
uri:f917aa20-16c5-4875-9206-1b5349505aae
UUID:
uuid:f917aa20-16c5-4875-9206-1b5349505aae
Local pid:
pubs:854566
Language:
English
Keywords:

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