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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
27
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pubmed:dateCreated |
2004-7-8
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pubmed:abstractText |
After ischemic stroke, partial recovery of function frequently occurs and may depend on the plasticity of axonal connections. Here, we examine whether blockade of the Nogo-NogoReceptor (NgR) pathway might enhance axonal sprouting and thereby recovery after focal brain infarction. Mutant mice lacking NgR or Nogo-AB recover complex motor function after stroke more completely than do control animals. After a stroke, greater numbers of axons emanating from the undamaged cortex cross the midline to innervate the contralateral red nucleus and the ipsilateral cervical spinal cord; this axonal plasticity is enhanced in ngr -/- or nogo-ab -/- mice. In rats with middle cerebral artery occlusion, both the recovery of motor skills and corticofugal axonal plasticity are promoted by intracerebroventricular administration of a function-blocking NgR fragment. Behavioral improvement occurs when therapy is initiated 1 week after arterial occlusion. Thus, delayed pharmacological blockade of the NgR promotes subacute stroke recovery by facilitating axonal plasticity.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/GPI-Linked Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nogo protein,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Peptide,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Rtn4r protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Rtn4r protein, rat
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1529-2401
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
7
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6209-17
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pubmed:dateRevised |
2011-8-29
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pubmed:meshHeading |
pubmed-meshheading:15240813-Animals,
pubmed-meshheading:15240813-Axons,
pubmed-meshheading:15240813-Behavior, Animal,
pubmed-meshheading:15240813-Disease Models, Animal,
pubmed-meshheading:15240813-GPI-Linked Proteins,
pubmed-meshheading:15240813-Infarction, Middle Cerebral Artery,
pubmed-meshheading:15240813-Male,
pubmed-meshheading:15240813-Mice,
pubmed-meshheading:15240813-Mice, Knockout,
pubmed-meshheading:15240813-Myelin Proteins,
pubmed-meshheading:15240813-Neuronal Plasticity,
pubmed-meshheading:15240813-Rats,
pubmed-meshheading:15240813-Rats, Sprague-Dawley,
pubmed-meshheading:15240813-Receptors, Cell Surface,
pubmed-meshheading:15240813-Receptors, Peptide,
pubmed-meshheading:15240813-Recombinant Fusion Proteins,
pubmed-meshheading:15240813-Recovery of Function,
pubmed-meshheading:15240813-Stroke,
pubmed-meshheading:15240813-Treatment Outcome
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pubmed:year |
2004
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pubmed:articleTitle |
Nogo receptor antagonism promotes stroke recovery by enhancing axonal plasticity.
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pubmed:affiliation |
Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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