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APP and APLP2 are essential at PNS and CNS synapses for transmission, spatial learning and LTP

Meyer, Sascha W (författare)
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Klevanski, Maja (författare)
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Delekate, Andrea (författare)
Cellular Neurobiology, Zoological Institute, TU Braunschweig, Braunschweig, Germany
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Voikar, Vootele (författare)
Institute of Anatomy and Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland
Aydin, Dorothee (författare)
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Hick, Meike (författare)
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Filippov, Mikhail (författare)
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Drost, Natalia (författare)
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Schaller, Kristin L (författare)
Department of Cell and Developmental Biology, Institute of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, CO, USA
Sarr, Martina (författare)
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Vogt, Miriam A (författare)
Department for Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany
Gass, Peter (författare)
Department of Biology, Institute of Human Movement Sciences, ETH Zurich, Zurich, Switzerland
Samanta, Ayan (författare)
Uppsala universitet,Polymerkemi,Department of Pharmaceutical Chemistry, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Jäschke, Andres (författare)
Department of Pharmaceutical Chemistry, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
Korte, Martin (författare)
Cellular Neurobiology, Zoological Institute, TU Braunschweig, Braunschweig, Germany
Wolfer, David P (författare)
Institute of Anatomy and Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland
John H, Caldwell (författare)
Department of Cell and Developmental Biology, Institute of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, CO, USA
Müller, Ulrike C (författare)
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany
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 (creator_code:org_t)
2011-04-26
2011
Engelska.
Ingår i: European Molecular Biology Organization. - : Wiley. - 1460-2075. ; 30, s. 2266-2280
Relaterad länk:
https://doi.org/10.1...
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https://doi.org/10.1...
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  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • Despite its key role in Alzheimer pathogenesis, the physiological function(s) of the amyloid precursor protein (APP) and its proteolytic fragments are still poorly understood. Previously, we generated APPsα knock‐in (KI) mice expressing solely the secreted ectodomain APPsα. Here, we generated double mutants (APPsα‐DM) by crossing APPsα‐KI mice onto an APLP2‐deficient background and show that APPsα rescues the postnatal lethality of the majority of APP/APLP2 double knockout mice. Surviving APPsα‐DM mice exhibited impaired neuromuscular transmission, with reductions in quantal content, readily releasable pool, and ability to sustain vesicle release that resulted in muscular weakness. We show that these defects may be due to loss of an APP/Mint2/Munc18 complex. Moreover, APPsα‐DM muscle showed fragmented post‐synaptic specializations, suggesting impaired postnatal synaptic maturation and/or maintenance. Despite normal CNS morphology and unaltered basal synaptic transmission, young APPsα‐DM mice already showed pronounced hippocampal dysfunction, impaired spatial learning and a deficit in LTP that could be rescued by GABAA receptor inhibition. Collectively, our data show that APLP2 and APP are synergistically required to mediate neuromuscular transmission, spatial learning and synaptic plasticity.

Ämnesord

NATURVETENSKAP  -- Biologi -- Biokemi och molekylärbiologi (hsv//swe)
NATURAL SCIENCES  -- Biological Sciences -- Biochemistry and Molecular Biology (hsv//eng)

Nyckelord

Alzheimer; amyloid precursor protein; knockout; learning; synaptic plasticity

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