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A role for SNAP25 in internalization of kainate receptors and synaptic plasticity

Otros títulosSNAP25 controls KAR endocytosis
AutorSelak, Sanja; Paternain, Ana V.; Aller, María Isabel; Picó, Esther; Rivera, Rocío; Lerma Gómez, Juan
Palabras claveKainate receptors (KARs)
Synaptic strength
Synaptic plasticity
GluK5 subunits
Protein complexes
Fecha de publicación13-ago-2009
CitaciónNeuron 63(3): 357-371 (2009)
ResumenRegulation of surface insertion and internalization of AMPA and NMDA receptors has emerged as a key mechanism for the control of synaptic strength. Regulatory elements for synaptic kainate receptors (KARs) are, however, largely undetermined. We have found that SNAP25 is critical for the synaptic removal of KARs, acting via GluK5 (i.e., KA2) subunits. SNAP25 coimmunoprecipitates with protein complexes containing PICK1, GRIP1, and GluK5 and colocalizes with GluK5 in both hippocampal neurons and transfected HEK293 cells. In hippocampal slices, purified SNAP25 antibodies and blocking peptides caused a GluK5-dependent run-up of KARs-mediated EPSC (EPSC-KAR) recorded from CA3 pyramidal neurons when included in the patch pipette and prevented activity-dependent long-term depression of EPSC-KAR. As EPSC-KAR LTD, SNAP25/PICK1/GluK5 interactions are dynamically regulated by PKC.
Descripción15 pages, 9 figures.-- PMID: 19679075 [PubMed].-- Supporting information including detailed Experimental Procedures and eight figures available at: http://dx.doi.org/10.1016/j.neuron.2009.07.017
Versión del editorhttp://dx.doi.org/10.1016/j.neuron.2009.07.017
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