| First Author | Corradi A | Year | 2008 |
| Journal | J Cell Sci | Volume | 121 |
| Issue | Pt 18 | Pages | 3042-51 |
| PubMed ID | 18713831 | Mgi Jnum | J:139688 |
| Mgi Id | MGI:3809368 | Doi | 10.1242/jcs.035063 |
| Citation | Corradi A, et al. (2008) Synapsin-I- and synapsin-II-null mice display an increased age-dependent cognitive impairment. J Cell Sci 121(Pt 18):3042-51 |
| abstractText | 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. |
