Impaired Synaptic Plasticity and Learning in Mice Lacking β-Adducin, an Actin-Regulating Protein.

Autor: Rabenstein, Rebecca L., Addy, Nii A., Caldarone, Barbara J., Yukiko Asaka, Gruenbaum, Lore M., Peters, Luanne L., Gilligan, Diana M., Fitzsimonds, Reiko M., Picciotto, Marina R.
Předmět:
Zdroj: Journal of Neuroscience; 2/23/2005, Vol. 25 Issue 8, p2138-2145, 8p, 3 Black and White Photographs, 2 Charts, 4 Graphs
Abstrakt: The adducin family of proteins interacts with the actin cytoskeleton and the plasma membrane in a calcium- and cAMP-dependent manner. Thus, adducins may be involved in changes in cytoskeletal organization resulting from synaptic stimulation. β-Adducin knockout mice were examined in physiological and behavioral paradigms related to synaptic plasticity to elucidate the role the adducin family plays in processes underlying learning and memory. In situ hybridization for α- and β-adducin demonstrates that these mRNAs are found throughout the brain, with high levels of expression in the hippocampus. Schaffer collateral-CA1 tetanic long-term potentiation decayed rapidly in acute hippocampal slices from β-adducin knock-out mice, although baseline spine morphology and postsynaptic density were normal. Interestingly, the input- output relationship was significantly increased in hippocampal slices from β-adducin knock-out mice. Furthermore, β-adducin knock-out mice were impaired in performance of fear conditioning and the water maze paradigm. The current results indicate that β-adducin may play an important role in the cellular mechanisms underlying activity-dependent synaptic plasticity associated with learning and memory. [ABSTRACT FROM AUTHOR]
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