Abnormal Long-Lasting Synaptic Plasticity and Cognition in Mice Lacking the Mental Retardation GenePak3
Copyright policy )Abnormal Long-Lasting Synaptic Plasticity and Cognition in Mice Lacking the Mental Retardation GenePak3
Mutations in thePak3gene lead to nonsyndromic mental retardation characterized by selective deficits in cognition. However, the underlying mechanisms are yet to be elucidated. We report here that the knock-out mice deficient in the expression of p21-activated kinase 3 (PAK3) exhibit significant abnormalities in synaptic plasticity, specifically hippocampal late-phase long-term potentiation, and deficiencies in learning and memory. A dramatic reduction in the active form of transcription factor cAMP-responsive element-binding protein in the knock-out mice implicates a novel signaling mechanism by which PAK3 and Rho signaling regulate synaptic function and cognition.
- University of Toronto Canada
- Hospital for Sick Children Canada
Brain Chemistry, Male, Mice, Knockout, Neurons, Memory Disorders, Neuronal Plasticity, Learning Disabilities, Conditioning, Classical, Long-Term Potentiation, Nerve Tissue Proteins, Dendrites, Hippocampus, Mice, Inbred C57BL, Mice, Intellectual Disability, Avoidance Learning, Animals, Cognition Disorders, Cyclic AMP Response Element-Binding Protein, Maze Learning
Brain Chemistry, Male, Mice, Knockout, Neurons, Memory Disorders, Neuronal Plasticity, Learning Disabilities, Conditioning, Classical, Long-Term Potentiation, Nerve Tissue Proteins, Dendrites, Hippocampus, Mice, Inbred C57BL, Mice, Intellectual Disability, Avoidance Learning, Animals, Cognition Disorders, Cyclic AMP Response Element-Binding Protein, Maze Learning
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