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000139736 0247_ $$2doi$$a10.1038/s41467-017-02415-1
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000139736 037__ $$aDZNE-2020-06058
000139736 041__ $$aEnglish
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000139736 1001_ $$0P:(DE-2719)2810594$$aChen, Xufeng$$b0$$eFirst author$$udzne
000139736 245__ $$aCKAMP44 modulates integration of visual inputs in the lateral geniculate nucleus.
000139736 260__ $$a[London]$$bNature Publishing Group UK$$c2018
000139736 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2018-01-17
000139736 264_1 $$2Crossref$$3print$$bSpringer Science and Business Media LLC$$c2018-12-01
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000139736 520__ $$aRelay neurons in the dorsal lateral geniculate nucleus (dLGN) receive excitatory inputs from retinal ganglion cells (RGCs). Retinogeniculate synapses are characterized by a prominent short-term depression of AMPA receptor (AMPAR)-mediated currents, but the underlying mechanisms and its function for visual integration are not known. Here we identify CKAMP44 as a crucial auxiliary subunit of AMPARs in dLGN relay neurons, where it increases AMPAR-mediated current amplitudes and modulates gating of AMPARs. Importantly, CKAMP44 is responsible for the distinctive short-term depression in retinogeniculate synapses by reducing the rate of recovery from desensitization of AMPARs. Genetic deletion of CKAMP44 strongly reduces synaptic short-term depression, which leads to increased spike probability of relay neurons when activated with high-frequency inputs from retinogeniculate synapses. Finally, in vivo recordings reveal augmented ON- and OFF-responses of dLGN neurons in CKAMP44 knockout (CKAMP44-/-) mice, demonstrating the importance of CKAMP44 for modulating synaptic short-term depression and visual input integration.
000139736 536__ $$0G:(DE-HGF)POF3-341$$a341 - Molecular Signaling (POF3-341)$$cPOF3-341$$fPOF III$$x0
000139736 542__ $$2Crossref$$i2018-01-17$$uhttp://creativecommons.org/licenses/by/4.0
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000139736 650_7 $$2NLM Chemicals$$aCKAMP44 protein, mouse
000139736 650_7 $$2NLM Chemicals$$aNerve Tissue Proteins
000139736 650_7 $$2NLM Chemicals$$aReceptors, AMPA
000139736 650_2 $$2MeSH$$aAnimals
000139736 650_2 $$2MeSH$$aElectroretinography
000139736 650_2 $$2MeSH$$aExcitatory Postsynaptic Potentials: physiology
000139736 650_2 $$2MeSH$$aFemale
000139736 650_2 $$2MeSH$$aGeniculate Bodies: cytology
000139736 650_2 $$2MeSH$$aGeniculate Bodies: metabolism
000139736 650_2 $$2MeSH$$aGeniculate Bodies: physiology
000139736 650_2 $$2MeSH$$aMice, Inbred C57BL
000139736 650_2 $$2MeSH$$aMice, Knockout
000139736 650_2 $$2MeSH$$aNerve Tissue Proteins: genetics
000139736 650_2 $$2MeSH$$aNerve Tissue Proteins: metabolism
000139736 650_2 $$2MeSH$$aNeurons: metabolism
000139736 650_2 $$2MeSH$$aNeurons: physiology
000139736 650_2 $$2MeSH$$aPhotic Stimulation
000139736 650_2 $$2MeSH$$aReceptors, AMPA: metabolism
000139736 650_2 $$2MeSH$$aRetina: cytology
000139736 650_2 $$2MeSH$$aRetina: metabolism
000139736 650_2 $$2MeSH$$aRetina: physiology
000139736 650_2 $$2MeSH$$aSynapses: physiology
000139736 650_2 $$2MeSH$$aSynaptic Transmission: genetics
000139736 650_2 $$2MeSH$$aSynaptic Transmission: physiology
000139736 7001_ $$0P:(DE-2719)2810579$$aAslam, Muhammad$$b1$$udzne
000139736 7001_ $$aGollisch, Tim$$b2
000139736 7001_ $$aAllen, Kevin$$b3
000139736 7001_ $$0P:(DE-2719)2810460$$aEngelhardt, Jakob$$b4$$eLast author$$udzne
000139736 77318 $$2Crossref$$3journal-article$$a10.1038/s41467-017-02415-1$$b : Springer Science and Business Media LLC, 2018-01-17$$n1$$p261$$tNature Communications$$v9$$x2041-1723$$y2018
000139736 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/s41467-017-02415-1$$gVol. 9, no. 1, p. 261$$n1$$p261$$q9:1<261$$tNature Communications$$v9$$x2041-1723$$y2018
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000139736 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC5772470
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