Synapsin-I- and synapsin-II-null mice display an increased age-dependent cognitive impairment
Synapsin I (SynI) and synapsin II (SynII) are major synaptic vesicle (SV) proteins that function in the regulation of the availability of SVs for release in mature neurons. SynI and SynII show a high level of sequence similarity and share many functions in vivo, although distinct physiological roles...
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Published in | Journal of cell science Vol. 121; no. 18; pp. 3042 - 3051 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
The Company of Biologists Limited
15.09.2008
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Subjects | |
Online Access | Get full text |
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Summary: | Synapsin I (SynI) and synapsin II (SynII) are major synaptic vesicle (SV) proteins that function in the regulation of the availability of SVs for release in mature neurons. SynI and SynII show a high level of sequence similarity and share many functions in vivo, although distinct physiological roles for the two proteins have been proposed. Both SynI⁻/⁻ and SynII⁻/⁻ mice have a normal lifespan, but exhibit a decreased number of SVs and synaptic depression upon high-frequency stimulation. Because of the role of the synapsin proteins in synaptic organization and plasticity, we studied the long-lasting effects of synapsin deletion on the phenotype of SynI⁻/⁻ and SynII⁻/⁻ mice during aging. Both SynI⁻/⁻ and SynII⁻/⁻ mice displayed behavioural defects that emerged during aging and involved emotional memory in both mutants, and spatial memory in SynII⁻/⁻ mice. These abnormalities, which were more pronounced in SynII⁻/⁻ mice, were associated with neuronal loss and gliosis in the cerebral cortex and hippocampus. The data indicate that SynI and SynII have specific and non-redundant functions, and that synaptic dysfunctions associated with synapsin mutations negatively modulate cognitive performances and neuronal survival during senescence. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0021-9533 1477-9137 |
DOI: | 10.1242/jcs.035063 |