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Neuronal Nogo‐A in the normal and post‐stroke brain
Author(s) -
Cheatwood Joseph L
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.307.6
Subject(s) - neuroscience , gene knockdown , stroke (engine) , inhibitory postsynaptic potential , central nervous system , neuroplasticity , myelin , knockout mouse , limiting , biology , receptor , cell culture , mechanical engineering , engineering , genetics , biochemistry
Originally identified as a component of central nervous system (CNS) myelin, we now know that Nogo‐A is expressed by a variety of cell types in the normal CNS, including neurons. The Nogo‐A protein is known to play a key role in limiting neuronal plasticity and functional recovery after stroke, but the precise mechanism of its inhibitory influence remains unknown. Post‐stroke administration of anti‐Nogo‐A antibodies results in functional recovery associated with lasting increases in dendritic complexity and spine density in key cortical areas. Due to the observable effects of anti‐Nogo‐A therapy on neurons, neuronal Nogo‐A represents a potential target for anti‐Nogo‐A therapeutics. Further, results of ongoing studies employing siRNA‐mediated knockdown of neuronal Nogo‐A and Nogo‐A knockout mice are beginning to yield important data on the functions of Nogo‐A in the intact and injured brain.