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Verfasst von:Dhawan, Serene [VerfasserIn]   i
 Myers, Philip [VerfasserIn]   i
 Bailey, David M. D. [VerfasserIn]   i
 Ostrovsky, Aaron [VerfasserIn]   i
 Evers, Jan-Felix [VerfasserIn]   i
 Landgraf, Matthias [VerfasserIn]   i
Titel:Reactive oxygen species mediate activity-regulated dendritic plasticity through NADPH oxidase and aquaporin regulation
Verf.angabe:Serene Dhawan, Philip Myers, David M.D. Bailey, Aaron D. Ostrovsky, Jan Felix Evers and Matthias Landgraf
E-Jahr:2021
Jahr:5 July 2021
Umfang:12 S.
Teil:volume:15
 year:2021
 elocationid:641802
 pages:1-12
 extent:12
Fussnoten:Gesehen am 08.09.2021
Titel Quelle:Enthalten in: Frontiers in cellular neuroscience
Ort Quelle:Lausanne : Frontiers Research Foundation, 2007
Jahr Quelle:2021
Band/Heft Quelle:15(2021), Artikel-ID 641802, Seite 1-12
ISSN Quelle:1662-5102
Abstract:Neurons utilize plasticity of dendritic arbors as part of a larger suite of adaptive plasticity mechanisms. This explicitly manifests with motoneurons in the Drosophila embryo and larva, where dendritic arbors are exclusively postsynaptic and are used as homeostatic devices, compensating for changes in synaptic input through adapting their growth and connectivity. We recently identified reactive oxygen species (ROS) as novel plasticity signals instrumental in this form of dendritic adjustment. ROS correlate with levels of neuronal activity and negatively regulate dendritic arbor size. Here, we investigated NADPH oxidases as potential sources of such activity-regulated ROS and implicate Dual Oxidase (but not Nox), which generates hydrogen peroxide extracellularly. We further show that the aquaporins Bib and Drip, but not Prip, are required for activity-regulated ROS-mediated adjustments of dendritic arbor size in motoneurons. These results suggest a model whereby neuronal activity leads to activation of the NADPH oxidase Dual Oxidase, which generates hydrogen peroxide at the extracellular face; aquaporins might then act as conduits that are necessary for these extracellular ROS to be channeled back into the cell where they negatively regulate dendritic arbor size.
DOI:doi:10.3389/fncel.2021.641802
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.3389/fncel.2021.641802
 Volltext: https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=DynamicDOIArticle&SrcApp=WOS&KeyAID=10.3389%2 ...
 DOI: https://doi.org/10.3389/fncel.2021.641802
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:aquaporins
 calcium
 dendrites
 Drosophila
 homeostatic plasticity
 hydrogen-peroxide
 kinase
 mechanisms
 modulation
 NADPH oxidases
 neurons
 oxidative stress
 plasticity
 reactive oxygen species
 redox regulation
 system
K10plus-PPN:1769701532
Verknüpfungen:→ Zeitschrift

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