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CKAMP44: a brain-specific protein attenuating short-term synaptic plasticity in the dentate gyrus

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von Engelhardt,  Jakob
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Mack,  Volker
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Seeburg,  Peter H.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Monyer,  Hannah
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

von Engelhardt, J., Mack, V., Sprengel, R., Kavenstock, N., Li, K. W., Stern-Bach, Y., et al. (2010). CKAMP44: a brain-specific protein attenuating short-term synaptic plasticity in the dentate gyrus. Science, 327(5972), 1518-1522. doi:10.1126/science.1184178.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002C-5FF1-2
Abstract
CKAMP44, identified here by a proteomic approach, is a brain-specific type I transmembrane protein that associates with AMPA receptors in synaptic spines. CKAMP44 expressed in Xenopus oocytes reduced GluA1- and A2-mediated steady-state currents, but did not affect kainate- or N-methyl-D-aspartate (NMDA) receptor-mediated currents. Mouse hippocampal CA1 pyramidal neurons expressed CKAMP44 at low abundance, and overexpression of CKAMP44 led to stronger and faster AMPA receptor desensitization, slower recovery from desensitization, and a reduction in the paired-pulse ratio of AMPA currents. By contrast, dentate gyrus granule cells exhibited strong CKAMP44 expression, and CKAMP44 knockout increased the paired-pulse ratio of AMPA currents in lateral and medial perforant path-granule cell synapses. CKAMP44 thus modulates short-term plasticity at specific excitatory synapses.