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CKAMP44 modulates integration of visual inputs in the lateral geniculate nucleus

Author

Listed:
  • Xufeng Chen

    (University Medical Center of the Johannes Gutenberg University Mainz
    German Center for Neurodegenerative Diseases (DZNE))

  • Muhammad Aslam

    (University Medical Center of the Johannes Gutenberg University Mainz
    German Center for Neurodegenerative Diseases (DZNE))

  • Tim Gollisch

    (University Medical Center Göttingen)

  • Kevin Allen

    (Medical Faculty of Heidelberg University and German Cancer Research Center (DKFZ))

  • Jakob Engelhardt

    (University Medical Center of the Johannes Gutenberg University Mainz
    German Center for Neurodegenerative Diseases (DZNE))

Abstract

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.

Suggested Citation

  • Xufeng Chen & Muhammad Aslam & Tim Gollisch & Kevin Allen & Jakob Engelhardt, 2018. "CKAMP44 modulates integration of visual inputs in the lateral geniculate nucleus," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02415-1
    DOI: 10.1038/s41467-017-02415-1
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