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Annotation

Jeans AF, Oliver PL, Johnson R, Capogna M, Vikman J, Molnár Z, Babbs A, Partridge CJ, Salehi A, Bengtsson M, Eliasson L, Rorsman P, Davies KE. A dominant mutation in Snap25 causes impaired vesicle trafficking, sensorimotor gating, and ataxia in the blind-drunk mouse. Proc Natl Acad Sci U S A . 2007 Feb 13 ; 104(7):2431-6. PubMed Abstract

Comments on Paper and Primary News
Comment by:  William HonerAlasdair Barr
Submitted 19 February 2007 Posted 19 February 2007

A New SNP for SNAP-25—An Animal Model of Schizophrenia?
SNAP-25 is one of the three core presynaptic proteins that combine to form the SNARE ternary complex, and as such, it plays a critical role in calcium-triggered exocytic transmitter release. There are two isoforms, SNAP-25A and SNAP-25B, which are highly homologous proteins that differ by only nine amino acids (Bark and Wilson, 1994). SNAP-23 represents another member of this protein family, which shares an approximately 60 percent identity with SNAP-25 (Ravichandran et al., 1996). Current theories of vesicular membrane fusion emphasize the role of SNARE proteins. According to these models, syntaxin 1, synaptobrevin (VAMP) 2 and SNAP-25 regulate neuroexocytosis by forming a complex that forces vesicle and plasma membranes together, allowing the transmitter contained in the synaptic vesicle to enter the synaptic cleft (  Read more


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Comment by:  Elizabeth Scarr
Submitted 12 March 2007 Posted 12 March 2007

The paper by Jeans et al. describes a viable mouse which carries a mutation (I67T) in the b isoform of SNAP-25, the blind-drunk mouse. Based primarily on the behavioral phenotype and on the results of two postmortem studies, the authors suggest that the line might be a suitable model for research into schizophrenia.

The mice show less frequent spontaneous release of glutamate than the wild-type, but the amplitude of the miniature excitatory postsynaptic currents were similar between genotypes. More severe deficits were seen with the release of glutamate in response to stimulation; the blind-drunk mice show a rapid decrease in synaptic transmission when high-frequency repetitive stimulation is applied, suggesting that these mice may have deficits in their ability to traffic synaptic vesicles.

Unlike the Coloboma mouse (a chromosomal deletion of 1-2cM near the distal end of Ch2 [Wilson, 2000], encompassing the gene for SNAP-25 amongst others), the blind-drunk mouse does not exhibit...  Read more


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