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

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Fältnamn	Indikatorer	Metadata
000		06250naa a2200565 4500
001		oai:DiVA.org:uu-373479
003		SwePub
008		190114s2011 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3734792 URI
024	7	a https://doi.org/10.1038/emboj.2011.1192 DOI
040		a (SwePub)uu
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Meyer, Sascha Wu Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
245	1 0	a APP and APLP2 are essential at PNS and CNS synapses for transmission, spatial learning and LTP
264		c 2011-04-26
264	1	b Wiley,c 2011
338		a electronic2 rdacarrier
520		a 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.
650	7	a NATURVETENSKAPx Biologix Biokemi och molekylärbiologi0 (SwePub)106022 hsv//swe
650	7	a NATURAL SCIENCESx Biological Sciencesx Biochemistry and Molecular Biology0 (SwePub)106022 hsv//eng
653		a Alzheimer; amyloid precursor protein; knockout; learning; synaptic plasticity
700	1	a Klevanski, Majau Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
700	1	a Delekate, Andreau Cellular Neurobiology, Zoological Institute, TU Braunschweig, Braunschweig, Germany4 aut
700	1	a Voikar, Vooteleu Institute of Anatomy and Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland4 aut
700	1	a Aydin, Dorotheeu Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
700	1	a Hick, Meikeu Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
700	1	a Filippov, Mikhailu Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
700	1	a Drost, Nataliau Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
700	1	a Schaller, Kristin Lu Department of Cell and Developmental Biology, Institute of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, CO, USA4 aut
700	1	a Sarr, Martinau Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
700	1	a Vogt, Miriam Au Department for Psychiatry and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany4 aut
700	1	a Gass, Peteru Department of Biology, Institute of Human Movement Sciences, ETH Zurich, Zurich, Switzerland4 aut
700	1	a Samanta, Ayanu Uppsala universitet,Polymerkemi,Department of Pharmaceutical Chemistry, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut0 (Swepub:uu)ayasa773
700	1	a Jäschke, Andresu Department of Pharmaceutical Chemistry, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
700	1	a Korte, Martinu Cellular Neurobiology, Zoological Institute, TU Braunschweig, Braunschweig, Germany4 aut
700	1	a Wolfer, David Pu Institute of Anatomy and Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland4 aut
700	1	a John H, Caldwellu Department of Cell and Developmental Biology, Institute of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, CO, USA4 aut
700	1	a Müller, Ulrike Cu Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germany4 aut
710	2	a Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Heidelberg, Germanyb Cellular Neurobiology, Zoological Institute, TU Braunschweig, Braunschweig, Germany4 org
773	0	t European Molecular Biology Organizationd : Wileyg 30, s. 2266-2280q 30<2266-2280x 1460-2075
773	0	t The EMBO Journald : Wileyg 30, s. 2266-2280q 30<2266-2280x 0261-4189
856	4	u https://doi.org/10.1038/emboj.2011.119y Fulltext
856	4	u http://emboj.embopress.org/content/30/11/2266
856	4	u https://uu.diva-portal.org/smash/get/diva2:1278596/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
856	4	u https://europepmc.org/articles/pmc3117640?pdf=render
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-373479
856	4 8	u https://doi.org/10.1038/emboj.2011.119

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