title: Reelin-immunoreactivity in the hippocampal formation of 9-month-old wildtype mouse: effects of APP/PS1 genotype and ovariectomy.
abstract: Reelin, an extracellular matrix protein has an important role in the migration, correct positioning and maturation of neurons during development. Though it is generally down-regulated in the postnatal period, expression of this large glycoprotein continues in the adult brain in some cell populations. In the present study, we examined the distribution of reelin-immunoreactivity (-ir) in the hippocampal formation of 9-month-old wildtype mice (WT). Then, reelin-ir in normal mice was compared to that of transgenic mice (APP/PS1) carrying mutated human APP and PS1 genes, which are linked to the familial form of Alzheimer's disease (AD). The APP/PS1 mice were additionally burdened with a second risk factor for AD, namely depletion of circulating gonadal hormones by ovariectomy (APP/PS1 + OVX). The analyses revealed that in adult WT reelin-ir is expressed by Cajal-Retzius cells and a subgroup of interneurons throughout the hippocampal formation. In addition, layer II projection neurons in the lateral entorhinal subfields are reelin-ir. Interestingly, ovariectomy decreases the number of reelin-ir cells in the hilus in WT mice, whereas AD-related genotype alone induces only a non-significant reduction. Unexpectedly, additional stress, e.g., depletion of gonadal hormones, does not aggravate the slight reduction in the reelin cell number in the APP/PS1 mice. We propose that the changes in normal reelin-ir are linked to disturbances in repair mechanisms in which APP/PS1 and gonadal hormones are involved and which are perturbed in neurodegenerative conditions, namely AD.
authors.affiliation: Department of Neuroscience and Neurology, University of Kuopio, Finland. riita.miettinen@uku.fi
authors.forename: Riitta
authors.initials: R
authors.lastname: Miettinen
authors.forename: Anett
authors.initials: A
authors.lastname: Riedel
authors.forename: Giedrius
authors.initials: G
authors.lastname: Kalesnykas
authors.forename: Hannu-Pekka
authors.initials: HP
authors.lastname: Kettunen
authors.forename: Jukka
authors.initials: J
authors.lastname: Puoliväli
authors.forename: Hilkka
authors.initials: H
authors.lastname: Soininen
authors.forename: Thomas
authors.initials: T
authors.lastname: Arendt
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D016564:Amyloid beta-Protein Precursor / Q000235:genetics*; D000818:Animals; D015816:Cell Adhesion Molecules, Neuronal / Q000378:metabolism*; D002452:Cell Count; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000235:genetics; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D012739:Gonadal Steroid Hormones / Q000378:metabolism*; D006624:Hippocampus / Q000033:anatomy & histology* / Q000166:cytology / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D008593:Menopause / Q000378:metabolism; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D010052:Ovariectomy; D053764:Presenilin-1; D000091042:Reelin Protein; D012697:Serine Endopeptidases / Q000378:metabolism*
chemical_list: D016564:Amyloid beta-Protein Precursor; D015816:Cell Adhesion Molecules, Neuronal; D016326:Extracellular Matrix Proteins; D012739:Gonadal Steroid Hormones; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; C508853:PSEN1 protein, human; D053764:Presenilin-1; D000091042:Reelin Protein; C000717127:RELN protein, human; C000717128:Reln protein, mouse; D012697:Serine Endopeptidases