title: Impaired synaptic plasticity and learning in mice lacking beta-adducin, an actin-regulating protein.
abstract: 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. beta-Adducin knock-out 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 alpha- and beta-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 beta-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 beta-adducin knock-out mice. Furthermore, beta-adducin knock-out mice were impaired in performance of fear conditioning and the water maze paradigm. The current results indicate that beta-adducin may play an important role in the cellular mechanisms underlying activity-dependent synaptic plasticity associated with learning and memory.
authors.affiliation: Interdepartmental Neuroscience Program, Yale University School of Medicine, New Haven, Connecticut 06508, USA.
authors.forename: Rebecca L
authors.initials: RL
authors.lastname: Rabenstein
authors.forename: Nii A
authors.initials: NA
authors.lastname: Addy
authors.forename: Barbara J
authors.initials: BJ
authors.lastname: Caldarone
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Asaka
authors.forename: Lore M
authors.initials: LM
authors.lastname: Gruenbaum
authors.forename: Luanne L
authors.initials: LL
authors.lastname: Peters
authors.forename: Diana M
authors.initials: DM
authors.lastname: Gilligan
authors.forename: Reiko M
authors.initials: RM
authors.lastname: Fitzsimonds
authors.forename: Marina R
authors.initials: MR
authors.lastname: Picciotto
mesh_terms: D000199:Actins / Q000378:metabolism*; D000818:Animals; D001362:Avoidance Learning / Q000502:physiology; D002148:Calmodulin-Binding Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D003214:Conditioning, Classical / Q000502:physiology; D003599:Cytoskeleton / Q000378:metabolism* / Q000648:ultrastructure; D003712:Dendrites / Q000648:ultrastructure; D004597:Electroshock; D005239:Fear / Q000502:physiology; D005260:Female; D046352:Freezing Reaction, Cataleptic / Q000502:physiology; D006179:Gyrus Cinguli / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D007859:Learning Disabilities / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D018782:Maze Learning / Q000502:physiology; D008569:Memory Disorders / Q000235:genetics* / Q000503:physiopathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008818:Mice, Neurologic Mutants; D009419:Nerve Tissue Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D009473:Neuronal Plasticity / Q000235:genetics / Q000502:physiology*; D009714:Nucleus Accumbens / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D000099291:Adducins
chemical_list: D000199:Actins; D002148:Calmodulin-Binding Proteins; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D000099291:Adducins
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