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The Journal of Neuroscience, May 6, 2009, 29(18):5884-5896; doi:10.1523/JNEUROSCI.5756-08.2009

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Behavioral/Systems/Cognitive
X11-Like Protein Deficiency Is Associated with Impaired Conflict Resolution in Mice

Yoshitake Sano,¹ Veravej G. Ornthanalai,² Kazuyuki Yamada,³ Chihiro Homma,³ Hitomi Suzuki,¹ Toshiharu Suzuki,⁴ Niall P. Murphy,² and Shigeyoshi Itohara¹

¹Laboratory for Behavioral Genetics, ²Molecular Neuropathology Group, and ³Research Resource Center, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan, and ⁴Laboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido 060-0812, Japan

Correspondence should be addressed to Shigeyoshi Itohara, Laboratory for Behavioral Genetics, RIKEN BSI, 2-1 Hirosawa, Wako 351-0198, Japan. Email: sitohara{at}brain.riken.jp

Understanding how emotion is generated, how conflicting emotions are regulated, and how emotional states relate to sophisticated behaviors is a crucial challenge in brain research. Model animals showing selective emotion-related phenotypes are highly useful for examining these issues. Here, we describe a novel mouse model that withdraws in approach-avoidance conflicts. X11-like (X11L)/Mint2 is a neuronal adapter protein with multiple protein-protein interaction domains that interacts with several proteins involved in modulating neuronal activity. X11L-knock-out (KO) mice were subordinate under competitive feeding conditions. X11L-KO mice lost significantly more weight than cohoused wild-type mice without signs of decreased motivation to eat or physical weakness. In a resident-intruder test, X11L-KO mice showed decreased intruder exploration behavior. Moreover, X11L-KO mice displayed decreased marble-burying, digging and burrowing behaviors, indicating aberrant ethological responses to attractive stimuli. In contrast, X11L-KO mice were indistinguishable from wild-type mice in the open field, elevated plus maze, and light/dark transition tests, which are often used to assess anxiety-like behavior. Neurochemical analysis revealed a monoamine imbalance in several forebrain regions. The defective ethological responses and social behaviors in X11L-KO mice were rescued by the expression of X11L under a Camk2a promoter using the Tet-OFF system during development. These findings suggest that X11L is involved in the development of neuronal circuits that contribute to conflict resolution.

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Received Dec. 3, 2008; revised March 12, 2009; accepted April 4, 2009.

Correspondence should be addressed to Shigeyoshi Itohara, Laboratory for Behavioral Genetics, RIKEN BSI, 2-1 Hirosawa, Wako 351-0198, Japan. Email: sitohara{at}brain.riken.jp

This article has been cited by other articles:

				J. C. Mitchell, B. B. Ariff, D. M. Yates, K.-F. Lau, M. S. Perkinton, B. Rogelj, J. D. Stephenson, C. C.J. Miller, and D. M. McLoughlin X11{beta} rescues memory and long-term potentiation deficits in Alzheimer's disease APPswe Tg2576 mice Hum. Mol. Genet., December 1, 2009; 18(23): 4492 - 4500. [Abstract] [Full Text] [PDF]

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