Synapsin-I- and synapsin-II-null mice display an increased age-dependent cognitive impairment

Anna Corradi, Alessio Zanardi, Caterina Giacomini, Franco Onofri, Flavia Valtorta, Michele Zoli, Fabio Benfenati

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)3042-3051
Number of pages10
JournalJournal of Cell Science
Volume121
Issue number18
DOIs
Publication statusPublished - Sep 15 2008

Keywords

  • Aging
  • Behaviour
  • Knock out
  • Learning and memory
  • Neurodegeneration
  • Synapsins

ASJC Scopus subject areas

  • Cell Biology

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