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The Journal of Neuroscience, July 13, 2005, 25(28):6641-6650; doi:10.1523/JNEUROSCI.0028-05.2005

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Development/Plasticity/Repair
Abnormal Long-Lasting Synaptic Plasticity and Cognition in Mice Lacking the Mental Retardation Gene Pak3

Jinsong Meng,^1,2,3 Yanghong Meng,^1,2,3 Amanda Hanna,⁴ Christopher Janus,^1,4 and Zhengping Jia^1,2,3

¹Brain and Behavior Program and ²Division of Neurology, The Hospital for Sick Children, Toronto, Ontario, Canada M5G 1X8, ³Department of Physiology, University of Toronto, and ⁴Center for Research in Neurodegenerative Diseases, Toronto, Ontario, Canada M5S 3H2

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.

Key words: mental retardation gene; Rho signaling; hippocampal LTP; CREB; learning and memory; actin

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Received Jan 4, 2005; revised June 2, 2005; accepted June 4, 2005.

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