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First published online 19 August 2008
doi: 10.1242/jcs.035063

Journal of Cell Science 121, 3042-3051 (2008)
Published by The Company of Biologists 2008
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Research Article

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

Anna Corradi1, Alessio Zanardi2, Caterina Giacomini1, Franco Onofri1, Flavia Valtorta3, Michele Zoli2 and Fabio Benfenati1,4,*

1 Department of Experimental Medicine, Section of Physiology, University of Genova and Istituto Nazionale di Neuroscienze, Viale Benedetto XV, 3 16132 Genova, Italy
2 Department of Biomedical Sciences, Section of Physiology, University of Modena, Via Campi 287, 41100 Modena, Italy
3 San Raffaele Scientific Institute/Vita-Salute University, IIT Unit of Molecular Neuroscience and Istituto Nazionale di Neuroscienze, via Olgettina 58, 20132 Milano, Italy
4 Department of Neuroscience and Brain Technologies, The Italian Institute of Technology, Via Morego 30, 16163 Genova, Italy

* Author for correspondence (e-mail: fabio.benfenati{at}unige.it)

Accepted 2 July 2008

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.

Key words: Synapsins, Aging, Knock out, Behaviour, Learning and memory, Neurodegeneration


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© The Company of Biologists Ltd 2008