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Publication : Abnormal long-lasting synaptic plasticity and cognition in mice lacking the mental retardation gene Pak3.

First Author  Meng J Year  2005
Journal  J Neurosci Volume  25
Issue  28 Pages  6641-50
PubMed ID  16014725 Mgi Jnum  J:99811
Mgi Id  MGI:3583863 Doi  10.1523/JNEUROSCI.0028-05.2005
Citation  Meng J, et al. (2005) Abnormal long-lasting synaptic plasticity and cognition in mice lacking the mental retardation gene Pak3. J Neurosci 25(28):6641-50
abstractText  Mutations in the Pak3 gene 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.
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