title: Deprivation-induced dendritic shrinkage might be oppositely affected by the expression of wild-type and mutated human amyloid precursor protein.
abstract: 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.
authors.affiliation: Department of Anatomy, Histology and Embryology, Semmelweis University Medical School, Budapest, Hungary. dralpar@gmx.net
authors.forename: Alán
authors.initials: A
authors.lastname: Alpár
authors.forename: Nicole
authors.initials: N
authors.lastname: Naumann
authors.forename: Uwe
authors.initials: U
authors.lastname: Ueberham
authors.forename: Thomas
authors.initials: T
authors.lastname: Arendt
authors.forename: Ulrich
authors.initials: U
authors.lastname: Gärtner
mesh_terms: D000344:Afferent Pathways / Q000503:physiopathology; D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000737:chemistry / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics*; D000818:Animals; D002454:Cell Differentiation / Q000235:genetics; D003072:Cognition Disorders / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D003712:Dendrites / Q000378:metabolism / Q000473:pathology*; D003714:Denervation; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D009410:Nerve Degeneration / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000235:genetics; D012683:Sensory Deprivation / Q000502:physiology*; D011984:Sensory Receptor Cells / Q000502:physiology; D013003:Somatosensory Cortex / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D014276:Trigeminal Nerve / Q000503:physiopathology; D014738:Vibrissae / Q000293:injuries / Q000502:physiology
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor