A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation

0346778 - ÚMG 2011 RIV GB eng J - Journal Article
Pavlowski, A. - Gianfelice, A. - Pallotto, M. - Zanchi, A. - Vara, H. - Khelfaoui, M. - Valnegri, P. - Rezai, X. - Bassani, S. - Brambilla, D. - Kumpošt, Jiří - Blahoš, Jaroslav - Roux, M.J. - Humeau, Y. - Chelly, J. - Passafaro, M. - Giustetto, M. - Billuart, P. - Sala, C.
A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation.
Current Biology. Roč. 20, č. 2 (2010), s. 103-115. ISSN 0960-9822. E-ISSN 1879-0445
R&D Projects: GA ČR GA303/08/1591
Institutional research plan: CEZ:AV0Z50520514
Keywords : synaptic plasticity * hippocampal neurons * PSD-95
Subject RIV: EB - Genetics ; Molecular Biology
Impact factor: 10.025, year: 2010

Here we show that IL1RAPL1 is present in dendritic spine where it interacts with PSD-95, a major component of excitatory postsynaptic compartment. Using gain- and loss-of-function experiments in neurons, we demonstrated that IL1RAPL1 regulates the synaptic localization of PSD-95 by controlling c-Jun terminal kinase (JNK) activity and PSD-95 phosphorylation. Mice carrying a null mutation of the mouse Il1rapl1 gene show a reduction of both dendritic spine density and excitatory synapses in the CA1 region of the hippocampus. These structural abnormalities are associated with specific deficits in hippocampal long-term synaptic plasticity.
Permanent Link: http://hdl.handle.net/11104/0187709