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Journal Article

Impairment of learning and memory in TAG-1 deficient mice associated with shorter CNS internodes and disrupted juxtaparanodes.

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84125

Panagiotaropoulos,  T
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Citation

Savvaki, M., Panagiotaropoulos, T., Stamatakis A, Sargiannidou I, Karatzioula P, Watanabe K, Stylianopoulou F, Karagogeos, D., & Kleopa, K. (2008). Impairment of learning and memory in TAG-1 deficient mice associated with shorter CNS internodes and disrupted juxtaparanodes. Molecular and Cellular Neuroscience, 39(3), 478-490. doi:10.1016/j.mcn.2008.07.025.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-C6A3-9
Abstract
The cell adhesion molecule TAG-1 is expressed by neurons and glial cells and plays a role in axon outgrowth, migration and fasciculation during development. TAG-1 is also required for the clustering of Kv1.1/1.2 potassium channels and Caspr2 at the juxtaparanodes of myelinated fibers. Behavioral examination of TAG-1 deficient mice (Tag-1amp;8722;/amp;8722;) showed cognitive impairments in the Morris water maze and novel object recognition tests, reduced spontaneous motor activity, abnormal gait coordination and increased response latency to noxious stimulation. Investigation at the molecular level revealed impaired juxtaparanodal clustering of Caspr2 and Kv1.1/1.2 in the hippocampus, entorhinal cortex, cerebellum and olfactory bulb, with diffusion into the internode. Caspr2 and Kv1.1 levels were reduced in the cerebellum and olfactory bulb. Moreover, Tag-1amp;8722;/amp;8722; mice had shorter internodes in the cerebral and cere bellar white mat ter. The detected molecular alterations may account for the behavioural deficits and hyperexcitability in these animals.