Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-8586
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dc.contributor.authorHetsch, Florian-
dc.contributor.authorWang, Danni-
dc.contributor.authorChen, Xufeng-
dc.contributor.authorZhang, Jiong-
dc.contributor.authorAslam, Muhammad-
dc.contributor.authorKegel, Marcel-
dc.contributor.authorTonner, Henrik-
dc.contributor.authorGrus, Franz-
dc.contributor.authorEngelhardt, Jakob von-
dc.date.accessioned2023-01-19T09:04:07Z-
dc.date.available2023-01-19T09:04:07Z-
dc.date.issued2022-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/8602-
dc.description.abstractRelay neurons of the dorsal lateral geniculate nucleus (dLGN) receive inputs from retinal ganglion cells via retinogeniculate synapses. These connections undergo pruning in the first 2 weeks after eye opening. The remaining connections are strengthened several-fold by the insertion of AMPA receptors (AMPARs) into weak or silent synapses. In this study, we found that the AMPAR auxiliary subunit CKAMP44 is required for receptor insertion and function of retinogeniculate synapses during development. Genetic deletion of CKAMP44 resulted in decreased synaptic strength and a higher number of silent synapses in young (P9–11) mice. Recovery from desensitisation of AMPARs was faster in CKAMP44 knockout (CKAMP44–/–) than in wild-type mice. Moreover, loss of CKAMP44 increased the probability of inducing plateau potentials, which are known to be important for eye-specific input segregation and retinogeniculate synapse maturation. The anatomy of relay neurons in the dLGN was changed in young CKAMP44–/– mice showing a transient increase in dendritic branching that normalised during later development (P26–33). Interestingly, input segregation in young CKAMP44–/– mice was not affected when compared to wild-type mice. These results demonstrate that CKAMP44 promotes maturation and modulates function of retinogeniculate synapses during early development of the visual system without affecting input segregation.en_GB
dc.description.sponsorshipGefördert durch die Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 491381577de
dc.language.isoengde
dc.rightsCC BY-NC*
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleCKAMP44 controls synaptic function and strength of relay neurons during early development of the dorsal lateral geniculate nucleusen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-8586-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleThe journal of physiologyde
jgu.journal.volume600de
jgu.journal.issue15de
jgu.pages.start3549de
jgu.pages.end3565de
jgu.publisher.year2022-
jgu.publisher.nameWiley-Blackwellde
jgu.publisher.placeHoboken, NJde
jgu.publisher.issn1469-7793de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1113/JP283172de
jgu.organisation.rorhttps://ror.org/023b0x485-
jgu.subject.dfgLebenswissenschaftende
Appears in collections:DFG-491381577-H

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