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The Journal of Neuroscience, February 2, 2005, 25(5):1081-1088; doi:10.1523/JNEUROSCI.2565.04.2005

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Cellular/Molecular
Age-Dependent Enhancement of Hippocampal Long-Term Potentiation and Impairment of Spatial Learning through the Rho-Associated Kinase Pathway in Protein Tyrosine Phosphatase Receptor Type Z-Deficient Mice

Kazue Niisato,^1,2 * Akihiro Fujikawa,^3 * Shoji Komai,^2 * Takafumi Shintani,³ Eiji Watanabe,³ Gaku Sakaguchi,⁴ Goro Katsuura,⁴ Toshiya Manabe,^1,2 and Masaharu Noda³

¹Division of Neuronal Network, Department of Basic Medical Sciences, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan, ²Division of Cell Biology and Neurophysiology, Department of Neuroscience, Faculty of Medicine, Kobe University, Chuo-ku, Kobe 650-0017, Japan, ³Division of Molecular Neurobiology, National Institute for Basic Biology, Myodaiji-cho, Okazaki 444-8787, Japan, and ⁴Discovery Research Laboratories, Shionogi and Company Ltd., Fukushima-ku, Osaka 553-0002, Japan

Although protein tyrosine phosphatases (PTPs) are expressed abundantly in the brain, their roles in synaptic plasticity have not been well elucidated. In this study, we have examined the physiological functions of Ptprz, which is a receptor-type PTP expressed predominantly in the brain as a chondroitin sulfate proteoglycan. We have examined phenotypes of mutant mice deficient in Ptprz using electrophysiological, pharmacological, and behavioral approaches. Mutant mice exhibit enhanced long-term potentiation (LTP) in the CA1 region of hippocampal slices and impaired spatial learning abilities in an age-dependent manner: young adult (<10 weeks old) mutant mice show normal LTP and learning abilities in the Morris water maze task, whereas adult (>13 weeks old) mutant mice exhibit enhanced LTP and impairment in the task. The enhanced LTP is specifically canceled out by pharmacological inhibition of Rho-associated kinase (ROCK), a major downstream effector of Rho. These findings suggest that the lack of Ptprz leads to aberrant activation of ROCK and resultantly to enhanced LTP in the slice and learning impairments in the animal.

Key words: tyrosine; phosphatase; synapse; memory; hippocampus; LTP

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Received June 29, 2004; revised December 4, 2004; accepted December 6, 2004.

This article has been cited by other articles:

				J. P. H. Chow, A. Fujikawa, H. Shimizu, R. Suzuki, and M. Noda Metalloproteinase- and {gamma}-Secretase-mediated Cleavage of Protein-tyrosine Phosphatase Receptor Type Z J. Biol. Chem., November 7, 2008; 283(45): 30879 - 30889. [Abstract] [Full Text] [PDF]

				T. Shintani and M. Noda Protein Tyrosine Phosphatase Receptor Type Z Dephosphorylates TrkA Receptors and Attenuates NGF-dependent Neurite Outgrowth of PC12 Cells J. Biochem., August 1, 2008; 144(2): 259 - 266. [Abstract] [Full Text] [PDF]

				A. Fujikawa, J. P. H. Chow, H. Shimizu, M. Fukada, R. Suzuki, and M. Noda Tyrosine Phosphorylation of ErbB4 is Enhanced by PSD95 and Repressed by Protein Tyrosine Phosphatase Receptor Type Z J. Biochem., September 1, 2007; 142(3): 343 - 350. [Abstract] [Full Text] [PDF]

				S. K. Olson, J. R. Bishop, J. R. Yates, K. Oegema, and J. D. Esko Identification of novel chondroitin proteoglycans in Caenorhabditis elegans: embryonic cell division depends on CPG-1 and CPG-2 J. Cell Biol., June 19, 2006; 173(6): 985 - 994. [Abstract] [Full Text] [PDF]

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