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The Journal of Neuroscience, March 7, 2007, 27(10):2513-2524; doi:10.1523/JNEUROSCI.4497-06.2007

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Development/Plasticity/Repair
Mice Deficient in Collapsin Response Mediator Protein-1 Exhibit Impaired Long-Term Potentiation and Impaired Spatial Learning and Memory

Kang-Yi Su,^1,2 Wei-Lin Chien,^3 * Wen-Mei Fu,³ I-Shing Yu,^2 * Hsiang-Po Huang,⁴ Pei-Hsing Huang,⁵ Shu-Rung Lin,⁸ Jin-Yuan Shih,⁶ Yi-Ling Lin,⁹ Yi-Ping Hsueh,⁹ Pan-Chyr Yang,⁶ and Shu-Wha Lin^2,7

¹Institute of Molecular Medicine, and Departments of ²Clinical Laboratory Sciences and Medical Biotechnology, ³Pharmacology, ⁴Medical Research, ⁵Pathology, ⁶Internal Medicine, and ⁷Laboratory Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei 100, Taiwan, ⁸Department of Bioscience Technology, College of Science, Chung-Yuan Christian University, Taoyuan 320, Taiwan, and ⁹Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan

Correspondence should be addressed to either of the following: Dr. Shu-Wha Lin, Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Number 7, Chung-San South Road, Taipei 100, Taiwan. Email: mtshuwha{at}ccms.ntu.edu.tw; or Dr. Pang-Chyr Yang, Department of Internal Medicine, College of Medicine, National Taiwan University, Number 7, Chung-San South Road, Taipei 100, Taiwan. Email: pcyang{at}ha.mc.ntu.edu.tw

Collapsing response mediator protein-1 (CRMP-1) was initially identified in brain and has been implicated in plexin-dependent neuronal function. The high amino acid sequence identity among the five CRMPs has hindered determination of the functions of each individual CRMP. We generated viable and fertile CRMP-1 knock-out (CRMP-1^–/–) mice with no evidence of gross abnormality in the major organs. CRMP-1^–/– mice exhibited intense microtubule-associated protein 2 (MAP2) staining in the proximal portion of the dendrites, but reduced and disorganized MAP2 staining in the distal dendrites of hippocampal CA1 pyramidal cells. Immunoreactivity to GAP-43 (growth-associated protein-43) and PSD95 (postsynaptic density-95) (a postsynaptic membrane adherent cytoskeletal protein) was also decreased in the CA1 region of the knock-out mice. These changes were consistent with the mutant mice showing a reduction in long-term potentiation (LTP) in the CA1 region and impaired performance in hippocampal-dependent spatial learning and memory tests. CRMP-1^–/– mice showed a normal synapsin I labeling pattern in CA1 and normal paired-pulse facilitation. These findings provide the first evidence suggesting that CRMP-1 may be involved in proper neurite outgrowth in the adult hippocampus and that loss of CRMP-1 may affect LTP maintenance and spatial learning and memory.

Key words: CRMP-1; knock-out mice; Cre recombinase; loxP; Morris water maze; long-term potentiation

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Received May 19, 2006; revised Jan. 23, 2007; accepted Jan. 23, 2007.

Correspondence should be addressed to either of the following: Dr. Shu-Wha Lin, Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Number 7, Chung-San South Road, Taipei 100, Taiwan. Email: mtshuwha{at}ccms.ntu.edu.tw; or Dr. Pang-Chyr Yang, Department of Internal Medicine, College of Medicine, National Taiwan University, Number 7, Chung-San South Road, Taipei 100, Taiwan. Email: pcyang{at}ha.mc.ntu.edu.tw

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