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Deprivation‐induced dendritic shrinkage might be oppositely affected by the expression of wild‐type and mutated human amyloid precursor protein
Author(s) -
Alpár Alán,
Naumann Nicole,
Ueberham Uwe,
Arendt Thomas,
Gärtner Ulrich
Publication year - 2009
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22008
Subject(s) - amyloid precursor protein , microbiology and biotechnology , neurite , wild type , mutant , biology , amyloid (mycology) , in vivo , synapse , synaptic plasticity , neuroscience , alzheimer's disease , in vitro , pathology , biochemistry , genetics , medicine , gene , receptor , botany , disease
The physiological role of the amyloid precursor protein (APP) and its proteolytic fragments in the brain is associated with neuronal survival, neurite outgrowth, synaptic formation, and neuronal plasticity. However, malregulation of APP processing leads to disordered balance of fragments, which may results in opposite, degenerative neuronal effects. In the present study, we analyzed in vivo effects of the expression of wild‐type or mutated human APP on afferent deprivation‐induced changes of dendritic morphology. After vibrissectomy, expression of wild‐type human APP prevented diameter shrinkage of dendritic segments as well as dendritic rarefaction of apical arbors. In contrast, mutant human APP expression exacerbated degenerative changes of deprived barrel neurons. Degradation of apical arbors was especially pronounced. Results demonstrate for the first time opposite effects of the expression of wild‐type and mutated human APP on deprivation‐induced dendritic restructuring in vivo. © 2009 Wiley‐Liss, Inc.