期刊
JOURNAL OF CELL SCIENCE
卷 121, 期 18, 页码 3042-3051出版社
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.035063
关键词
synapsins; aging; knock out; behaviour; learning and memory; neurodegeneration
类别
资金
- Ministry of the University and Research Grants [PRIN 2006]
- Compagnia di San Paolo
- Telethon-Italy [GCP05134]
- Cariplo Foundation
- Fondazione Mariani
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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