Source:http://linkedlifedata.com/resource/pubmed/id/19449316
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2009-7-2
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pubmed:abstractText |
The development of nervous system connectivity depends upon the arborization of dendritic fields and the stabilization of dendritic spine synapses. It is well established that neuronal activity and the neurotrophin BDNF modulate these correlated processes. However, the downstream mechanisms by which these extrinsic signals regulate dendritic development and spine stabilization are less well known. Here we report that a substrate of BDNF signaling, the Ankyrin Repeat-rich Membrane Spanning (ARMS) protein or Kidins220, plays a critical role in the branching of cortical and hippocampal dendrites and in the turnover of cortical spines. In the barrel somatosensory cortex and the dentate gyrus, regions where ARMS/Kidins220 is highly expressed, no difference in the complexity of dendritic arbors was observed in 1-month-old adolescent ARMS/Kidins220(+/-) mice compared to wild-type littermates. However, at 3 months of age, young adult ARMS/Kidins220(+/-) mice exhibited decreased dendritic complexity. This suggests that ARMS/Kidins220 does not play a significant role in the initial formation of dendrites but, rather, is involved in the refinement or stabilization of the arbors later in development. In addition, at 1 month of age, the rate of spine elimination was higher in ARMS/Kidins220(+/-) mice than in wild-type mice, suggesting that ARMS/Kidins220(+/-) levels regulate spine stability. Taken together, these data suggest that ARMS/Kidins220 is important for the growth of dendritic arbors and spine stability during an activity- and BDNF-dependent period of development.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Brain-Derived Neurotrophic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Luminescent Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Microtubule-Associated Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mtap2 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1932-8451
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pubmed:author | |
pubmed:copyrightInfo |
(c) 2009 Wiley Periodicals, Inc. Develop Neurobiol 2009.
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pubmed:issnType |
Print
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pubmed:volume |
69
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
547-57
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pubmed:dateRevised |
2011-4-28
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pubmed:meshHeading |
pubmed-meshheading:19449316-Age Factors,
pubmed-meshheading:19449316-Animals,
pubmed-meshheading:19449316-Ankyrin Repeat,
pubmed-meshheading:19449316-Brain-Derived Neurotrophic Factor,
pubmed-meshheading:19449316-Cells, Cultured,
pubmed-meshheading:19449316-Cerebral Cortex,
pubmed-meshheading:19449316-Dendritic Spines,
pubmed-meshheading:19449316-Embryo, Mammalian,
pubmed-meshheading:19449316-Female,
pubmed-meshheading:19449316-Gene Expression Regulation, Developmental,
pubmed-meshheading:19449316-Hippocampus,
pubmed-meshheading:19449316-Luminescent Proteins,
pubmed-meshheading:19449316-Male,
pubmed-meshheading:19449316-Membrane Proteins,
pubmed-meshheading:19449316-Mice,
pubmed-meshheading:19449316-Mice, Inbred C57BL,
pubmed-meshheading:19449316-Mice, Transgenic,
pubmed-meshheading:19449316-Microtubule-Associated Proteins,
pubmed-meshheading:19449316-Mutation,
pubmed-meshheading:19449316-Neurites,
pubmed-meshheading:19449316-Neurons,
pubmed-meshheading:19449316-Rats,
pubmed-meshheading:19449316-Rats, Sprague-Dawley,
pubmed-meshheading:19449316-Silver Staining
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pubmed:year |
2009
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pubmed:articleTitle |
Ankyrin Repeat-rich Membrane Spanning/Kidins220 protein regulates dendritic branching and spine stability in vivo.
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pubmed:affiliation |
Molecular Neurobiology Program, Skirball Institute of Biomolecular Medicine, Department of Physiology and Neuroscience, New York University School of Medicine, New York, New York 10016, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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