References
Query Results -- Details
MGI Accession ID: MGI:3057254
J Number: J:93544
Other Accession IDs:
Title: Double-knockout mice for alpha- and beta-synucleins: effect on synaptic functions.
Authors: Chandra S; Fornai F; Kwon HB; Yazdani U; Atasoy D; Liu X; Hammer RE; Battaglia G; German DC; Castillo PE; Sudhof TC
Journal: Proc Natl Acad Sci U S A
Volume: 101
Issue: 41
Date: 2004 Oct 12
Year: 2004
Pages: 14966-71
Review Status: Peer Reviewed
Abstract:
An abundant presynaptic protein, alpha-synuclein, is centrally involved in the pathogenesis of Parkinson's disease. However, conflicting data exist about the normal function of alpha-synuclein, possibly because alpha-synuclein is redundant with the very similar beta-synuclein. To investigate the functions of synucleins systematically, we have now generated single- and double-knockout (KO) mice that lack alpha- and/or beta-synuclein. We find that deletion of synucleins in mice does not impair basic brain functions or survival. We detected no significant changes in the ultrastructure of synuclein-deficient synapses, in short- or long-term synaptic plasticity, or in the pool size or replenishment of recycling synaptic vesicles. However, protein quantitations revealed that KO of synucleins caused selective changes in two small synaptic signaling proteins, complexins and 14-3-3 proteins. Moreover, we found that dopamine levels in the brains of double-KO but not single-KO mice were decreased by approximately 20%. In contrast, serotonin levels were unchanged, and dopamine uptake and release from isolated nerve terminals were normal. These results show that synucleins are not essential components of the basic machinery for neurotransmitter release but may contribute to the long-term regulation and/or maintenance of presynaptic function.
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