These authors contributed equally to this work and should be considered joint first authors.
β-adducin (Add2) KO mice show synaptic plasticity, motor coordination and behavioral deficits accompanied by changes in the expression and phosphorylation levels of the α- and γ-adducin subunits
Article first published online: 22 SEP 2009
© 2009 International Centre for Genetic Engineering and Biotechnology. Journal compilation © 2009 Blackwell Publishing Ltd/International Behavioural and Neural Genetics Society
Genes, Brain and Behavior
Volume 9, Issue 1, pages 84–96, February 2010
How to Cite
Porro, F., Rosato-Siri, M., Leone, E., Costessi, L., Iaconcig, A., Tongiorgi, E. and Muro, A. F. (2010), β-adducin (Add2) KO mice show synaptic plasticity, motor coordination and behavioral deficits accompanied by changes in the expression and phosphorylation levels of the α- and γ-adducin subunits. Genes, Brain and Behavior, 9: 84–96. doi: 10.1111/j.1601-183X.2009.00537.x
- Issue published online: 28 JAN 2010
- Article first published online: 22 SEP 2009
- Received 8 April 2009, revised 9 June 2009, 19 August 2009, 26 August 2009 and 31 August 2009, accepted for publication 7 September 2009
- somatodendritic localization
Adducins are a family of proteins found in cytoskeleton junctional complexes, which bind and regulate actin filaments and actin-spectrin complexes. In brain, adducin is expressed at high levels and is identified as a constituent of synaptic structures, such as dendritic spines and growth cones of neurons. Adducin-induced changes in dendritic spines are involved in activity-dependent synaptic plasticity processes associated with learning and memory, but the mechanisms underlying these functions remain to be elucidated. Here, β-adducin knockout (KO) mice were used to obtain a deeper insight into the role of adducin in these processes. We showed that β-adducin KO mice showed behavioral, motor coordination and learning deficits together with an altered expression and/or phosphorylation levels of α-adducin and γ-adducin. We found that β-adducin KO mice exhibited deficits in learning and motor performances associated with an impairment of long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus. These effects were accompanied by a decrease in phosphorylation of adducin, a reduction in α-adducin expression levels and upregulation of γ-adducin in hippocampus, cerebellum and neocortex of mutant mice. In addition, we found that the mRNA encoding β-adducin is also located in dendrites, where it may participate in the fine modulation of LTP and LTD. These results strongly suggest coordinated expression and phosphorylation of adducin subunits as a key mechanism underlying synaptic plasticity, motor coordination performance and learning behaviors.