The Blind-Drunk Mutant Mouse: A Model for Schizophrenia?
Wellcome Trust Sanger Institute
Francis Crick Auditorium, Wellcome Trust Conference Centre, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1RQ, UK
19 November 2009 - 12midday
A discussion introduced by Professor Kay Davies, Head of Physiology, Anatomy and Genetics at the University of Oxford and Honorary Director of the Functional Genomics Unit at the Medical Research Council.
The SNARE protein complex is essential for synaptic vesicle exocytosis, but its study has been limited by the lethality of mouse knockouts. The viable blind-drunk mutant mouse, containing a point mutation in core SNARE protein Snap-25, has been identified and characterised. The blind-drunk mutation causes increased binding affinities in the SNARE complex, resulting in an impairment of normal exocytotic vesicle recycling. Such mice also display ataxia and impaired sensoimotor gating, a phenotype associated with psychiatric disorders in humans, and circadian abnormalities similar to schizophrenia patients. These studies therefore provide new insights, not possible using a gene knockout model, into the role of the SNARE complex in psychiatric disease.
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