dc.contributor.author
Barro-Soria, Rene
dc.contributor.author
Caicedo, Alejandro
dc.contributor.author
Jägle, Herbert
dc.contributor.author
Merkel, Laura
dc.contributor.author
Zhao, Na
dc.contributor.author
Knop, Gabriel
dc.contributor.author
Gierke, Kaspar
dc.contributor.author
Dannullis, Andrea
dc.contributor.author
Castrop, Hayo
dc.contributor.author
Brandstätter, Johann Helmut
dc.contributor.author
Kirchhoff, Frank
dc.contributor.author
Feigenspan, Andreas
dc.contributor.author
Strauß, Olaf
dc.date.accessioned
2020-01-08T10:41:19Z
dc.date.available
2020-01-08T10:41:19Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/26343
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-26103
dc.description.abstract
Fast, precise and sustained neurotransmission requires graded Ca2+ signals at the presynaptic terminal. Neurotransmitter release depends on a complex interplay of Ca2+ fluxes and Ca2+ buffering in the presynaptic terminal that is not fully understood. Here, we show that the angiotensin-receptor-associated protein (ATRAP) localizes to synaptic terminals throughout the central nervous system. In the retinal photoreceptor synapse and the cerebellar mossy fiber-granule cell synapse, we find that ATRAP is involved in the generation of depolarization-evoked synaptic Ca2+ transients. Compared to wild type, Ca2+ imaging in acutely isolated preparations of the retina and the cerebellum from ATRAP knockout mice reveals a significant reduction of the sarcoendoplasmic reticulum (SR) Ca2+-ATPase (SERCA) activity. Thus, in addition to its conventional role in angiotensin signaling, ATRAP also modulates presynaptic Ca2+ signaling within the central nervous system.
en
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject
angiotensin-receptor-associated protein
en
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit
dc.title
Angiotensin-Receptor-Associated Protein Modulates Ca2+ Signals in Photoreceptor and Mossy Fiber cells
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
19622
dcterms.bibliographicCitation.doi
10.1038/s41598-019-55380-8
dcterms.bibliographicCitation.journaltitle
Scientific Reports
dcterms.bibliographicCitation.number
1
dcterms.bibliographicCitation.originalpublishername
Nature Publishing Group
dcterms.bibliographicCitation.volume
9
refubium.affiliation
Charité - Universitätsmedizin Berlin
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.bibliographicCitation.pmid
31873081
dcterms.isPartOf.eissn
2045-2322