DIP/WISH deficiency enhances synaptic function and performance in the Barnes maze
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* Corresponding author: Tomoko Fukumi-Tominaga ttfukumi@hotmail.com
1 Neuroscience & Mental Health Program, The Hospital for Sick Children, Toronto, Canada
2 Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), Okazaki, Japan
3 Center for Genetic Analysis of Behavior, National Institute for Physiological Sciences, Okazaki, Japan
4 Department of Physiological Sciences, The Graduate University for Advanced Studies, Okazaki, Japan
Molecular Brain 2011, 4:39 doi:10.1186/1756-6606-4-39
Published: 21 October 2011Abstract
Background
DIP (diaphanous interacting protein)/WISH (WASP interacting SH3 protein) is a protein involved in cytoskeletal signaling which regulates actin cytoskeleton dynamics and/or microtubules mainly through the activity of Rho-related proteins. Although it is well established that: 1) spine-head volumes change dynamically and reflect the strength of the synapse accompanying long-term functional plasticity of glutamatergic synaptic transmission and 2) actin organization is critically involved in spine formation, the involvement of DIP/WISH in these processes is unknown.
Results
We found that DIP/WISH-deficient hippocampal CA1 neurons exhibit enhanced long-term potentiation via modulation of both pre- and post-synaptic events. Consistent with these electrophysiological findings, DIP/WISH-deficient mice, particularly at a relatively young age, found the escape hole more rapidly in the Barnes maze test.
Conclusions
We conclude that DIP/WISH deletion improves performance in the Barnes maze test in mice probably through increased hippocampal long-term potentiation.