001     139736
005     20240511120151.0
024 7 _ |a 10.1038/s41467-017-02415-1
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037 _ _ |a DZNE-2020-06058
041 _ _ |a English
082 _ _ |a 500
100 1 _ |a Chen, Xufeng
|0 P:(DE-2719)2810594
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|e First author
|u dzne
245 _ _ |a CKAMP44 modulates integration of visual inputs in the lateral geniculate nucleus.
260 _ _ |a [London]
|c 2018
|b Nature Publishing Group UK
264 _ 1 |3 online
|2 Crossref
|b Springer Science and Business Media LLC
|c 2018-01-17
264 _ 1 |3 print
|2 Crossref
|b Springer Science and Business Media LLC
|c 2018-12-01
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Relay 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.
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542 _ _ |i 2018-01-17
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|u http://creativecommons.org/licenses/by/4.0
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650 _ 7 |a CKAMP44 protein, mouse
|2 NLM Chemicals
650 _ 7 |a Nerve Tissue Proteins
|2 NLM Chemicals
650 _ 7 |a Receptors, AMPA
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Electroretinography
|2 MeSH
650 _ 2 |a Excitatory Postsynaptic Potentials: physiology
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Geniculate Bodies: cytology
|2 MeSH
650 _ 2 |a Geniculate Bodies: metabolism
|2 MeSH
650 _ 2 |a Geniculate Bodies: physiology
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Knockout
|2 MeSH
650 _ 2 |a Nerve Tissue Proteins: genetics
|2 MeSH
650 _ 2 |a Nerve Tissue Proteins: metabolism
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Neurons: physiology
|2 MeSH
650 _ 2 |a Photic Stimulation
|2 MeSH
650 _ 2 |a Receptors, AMPA: metabolism
|2 MeSH
650 _ 2 |a Retina: cytology
|2 MeSH
650 _ 2 |a Retina: metabolism
|2 MeSH
650 _ 2 |a Retina: physiology
|2 MeSH
650 _ 2 |a Synapses: physiology
|2 MeSH
650 _ 2 |a Synaptic Transmission: genetics
|2 MeSH
650 _ 2 |a Synaptic Transmission: physiology
|2 MeSH
700 1 _ |a Aslam, Muhammad
|0 P:(DE-2719)2810579
|b 1
|u dzne
700 1 _ |a Gollisch, Tim
|b 2
700 1 _ |a Allen, Kevin
|b 3
700 1 _ |a Engelhardt, Jakob
|0 P:(DE-2719)2810460
|b 4
|e Last author
|u dzne
773 1 8 |a 10.1038/s41467-017-02415-1
|b : Springer Science and Business Media LLC, 2018-01-17
|n 1
|p 261
|3 journal-article
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|t Nature Communications
|v 9
|y 2018
|x 2041-1723
773 _ _ |a 10.1038/s41467-017-02415-1
|g Vol. 9, no. 1, p. 261
|0 PERI:(DE-600)2553671-0
|n 1
|q 9:1<261
|p 261
|t Nature Communications
|v 9
|y 2018
|x 2041-1723
856 4 _ |y OpenAccess
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856 4 _ |y OpenAccess
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856 7 _ |2 Pubmed Central
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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913 1 _ |a DE-HGF
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21