Horn2013

Référence

Horn, K.E., Glasgow, S.D., Gobert, D., Bull, S.-J., Luk, T., Girgis, J., Tremblay, M.-E., McEachern, D., Bouchard, J.-F., Haber, M., Hamel, E., Krimpenfort, P., Murai, K., Berns, A., Doucet, G., Chapman, C.A., Ruthazer, E. and Kennedy, (2013) Expression by Neurons Regulates Synaptic Plasticity in the Adult Brain. Cell Reports, 3(1):173-185. (URL )

Résumé

Summary The transmembrane protein deleted in colorectal cancer (DCC) and its ligand, netrin-1, regulate synaptogenesis during development, but their function in the mature central nervous system is unknown. Given that {DCC} promotes cell-cell adhesion, is expressed by neurons, and activates proteins that signal at synapses, we hypothesized that {DCC} expression by neurons regulates synaptic function and plasticity in the adult brain. We report that {DCC} is enriched in dendritic spines of pyramidal neurons in wild-type mice, and we demonstrate that selective deletion of {DCC} from neurons in the adult forebrain results in the loss of long-term potentiation (LTP), intact long-term depression, shorter dendritic spines, and impaired spatial and recognition memory. {LTP} induction requires Src activation of {NMDA} receptor (NMDAR) function. {DCC} deletion severely reduced Src activation. We demonstrate that enhancing {NMDAR} function or activating Src rescues {LTP} in the absence of DCC. We conclude that {DCC} activation of Src is required for NMDAR-dependent {LTP} and certain forms of learning and memory.

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@ARTICLE { Horn2013,
    AUTHOR = { Horn, K.E. and Glasgow, S.D. and Gobert, D. and Bull, S.-J. and Luk, T. and Girgis, J. and Tremblay, M.-E. and McEachern, D. and Bouchard, J.-F. and Haber, M. and Hamel, E. and Krimpenfort, P. and Murai, K. and Berns, A. and Doucet, G. and Chapman, C.A. and Ruthazer, E. and Kennedy, },
    TITLE = { Expression by Neurons Regulates Synaptic Plasticity in the Adult Brain },
    JOURNAL = { Cell Reports },
    YEAR = { 2013 },
    VOLUME = { 3 },
    PAGES = { 173-185 },
    NUMBER = { 1 },
    ABSTRACT = { Summary The transmembrane protein deleted in colorectal cancer (DCC) and its ligand, netrin-1, regulate synaptogenesis during development, but their function in the mature central nervous system is unknown. Given that \{DCC\} promotes cell-cell adhesion, is expressed by neurons, and activates proteins that signal at synapses, we hypothesized that \{DCC\} expression by neurons regulates synaptic function and plasticity in the adult brain. We report that \{DCC\} is enriched in dendritic spines of pyramidal neurons in wild-type mice, and we demonstrate that selective deletion of \{DCC\} from neurons in the adult forebrain results in the loss of long-term potentiation (LTP), intact long-term depression, shorter dendritic spines, and impaired spatial and recognition memory. \{LTP\} induction requires Src activation of \{NMDA\} receptor (NMDAR) function. \{DCC\} deletion severely reduced Src activation. We demonstrate that enhancing \{NMDAR\} function or activating Src rescues \{LTP\} in the absence of DCC. We conclude that \{DCC\} activation of Src is required for NMDAR-dependent \{LTP\} and certain forms of learning and memory. },
    DOI = { http://dx.doi.org/10.1016/j.celrep.2012.12.005 },
    ISSN = { 2211-1247 },
    URL = { http://www.sciencedirect.com/science/article/pii/S2211124712004299 },
}

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