Abnormal Long-Lasting Synaptic Plasticity and Cognition in Mice Lacking the Mental Retardation GenePak3
| Autor: | Christopher Janus, Zhengping Jia, Yanghong Meng, Jinsong Meng, Amanda Hanna |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Male
rho GTP-Binding Proteins Development/Plasticity/Repair Conditioning Classical Long-Term Potentiation Nerve Tissue Proteins Protein Serine-Threonine Kinases Hippocampal formation CREB Hippocampus Mice Intellectual Disability Avoidance Learning Animals Phosphorylation Cyclic AMP Response Element-Binding Protein Maze Learning Transcription factor Brain Chemistry Mice Knockout Neurons Memory Disorders Neuronal Plasticity biology Learning Disabilities General Neuroscience Cognition Long-term potentiation Dendrites Mice Inbred C57BL Synaptic fatigue p21-Activated Kinases Synaptic plasticity biology.protein Memory consolidation Cognition Disorders Psychology Protein Processing Post-Translational Neuroscience Signal Transduction |
| Zdroj: | The Journal of Neuroscience. 25:6641-6650 |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/jneurosci.0028-05.2005 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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