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Titel: Alix is required for activity-dependent bulk endocytosis at brain synapses
VerfasserIn: Laporte, Marine H.
Chi, Kwang I.l.
Caudal, Laura C.
Zhao, Na
Schwarz, Yvonne
Rolland, Marta
Martinez-Hernandez, José
Martineau, Magalie
Chatellard, Christine
Denarier, Eric
Mercier, Vincent
Lemaître, Florent
Blot, Béatrice
Moutaux, Eve
Cazorla, Maxime
Perrais, David
Lanté, Fabien
Bruns, Dieter
Fraboulet, Sandrine
Hemming, Fiona J.
Kirchhoff, Frank
Sadoul, Rémy
Sprache: Englisch
Titel: PLoS Biology
Bandnummer: 20
Heft: 6
Verlag/Plattform: PLOS
Erscheinungsjahr: 2022
DDC-Sachgruppe: 610 Medizin, Gesundheit
Dokumenttyp: Journalartikel / Zeitschriftenartikel
Abstract: In chemical synapses undergoing high frequency stimulation, vesicle components can be retrieved from the plasma membrane via a clathrin-independent process called activitydependent bulk endocytosis (ADBE). Alix (ALG-2-interacting protein X/PDCD6IP) is an adaptor protein binding to ESCRT and endophilin-A proteins which is required for clathrinindependent endocytosis in fibroblasts. Alix is expressed in neurons and concentrates at synapses during epileptic seizures. Here, we used cultured neurons to show that Alix is recruited to presynapses where it interacts with and concentrates endophilin-A during conditions triggering ADBE. Using Alix knockout (ko) neurons, we showed that this recruitment, which requires interaction with the calcium-binding protein ALG-2, is necessary for ADBE. We also found that presynaptic compartments of Alix ko hippocampi display subtle morphological defects compatible with flawed synaptic activity and plasticity detected electrophysiologically. Furthermore, mice lacking Alix in the forebrain undergo less seizures during kainate-induced status epilepticus and reduced propagation of the epileptiform activity. These results thus show that impairment of ADBE due to the lack of neuronal Alix leads to abnormal synaptic recovery during physiological or pathological repeated stimulations.
DOI der Erstveröffentlichung: 10.1371/journal.pbio.3001659
URL der Erstveröffentlichung: https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3001659
Link zu diesem Datensatz: urn:nbn:de:bsz:291--ds-370791
hdl:20.500.11880/33658
http://dx.doi.org/10.22028/D291-37079
ISSN: 1545-7885
Datum des Eintrags: 25-Aug-2022
Bezeichnung des in Beziehung stehenden Objekts: Supporting information
In Beziehung stehendes Objekt: https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s001
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s002
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s003
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s004
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s005
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s006
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s007
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s008
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s009
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s010
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s011
https://journals.plos.org/plosbiology/article/file?type=supplementary&id=10.1371/journal.pbio.3001659.s012
Fakultät: M - Medizinische Fakultät
Fachrichtung: M - Physiologie
Professur: M - Prof. Dr. Frank Kirchhoff
Sammlung:SciDok - Der Wissenschaftsserver der Universität des Saarlandes

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