Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/216971
COMPARTIR / EXPORTAR:
logo share SHARE logo core CORE BASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE

Invitar a revisión por pares abierta
Título

Activity dependent internalization of the glutamate transporter GLT-1 requires calcium entry through the NCX sodium/calcium exchanger

AutorIbáñez, Ignacio CSIC; Bartolomé-Martín, David; Piniella, Dolores; Giménez, Cecilio; Zafra, Francisco CSIC ORCID
Palabras claveIntracellular trafficking
Endocytosis
Glutamate
Calcium
Transpor
Fecha de publicación21-mar-2019
CitaciónNeurochemistry International 123: 125- 132 (2019)
ResumenGLT-1 is the main glutamate transporter in the brain and its trafficking controls its availability at the cell surface, thereby shaping glutamatergic neurotransmission under physiological and pathological conditions. Extracellular glutamate is known to trigger ubiquitin-dependent GLT-1 internalization from the surface of the cell to the intracellular compartment, yet here we show that internalization also requires the participation of calcium ions. Consistent with previous studies, the addition of glutamate (1 mM) to mixed primary cultures (containing neurons and astrocytes) promotes GLT-1 internalization, an effect that was suppressed in the absence of extracellular Ca. The pathways of Ca mobilization by astrocytes were analyzed in these mixed cultures using the genetically encoded calcium sensor GCaMP6f. A complex pattern of calcium entry was activated by glutamate, with a dramatic and rapid rise in the intracellular Ca concentration partially driven by glutamate transporters, especially in the initial stages after exposure to glutamate. The Na/Ca exchanger (NCX) plays a dominant role in this Ca mobilization and its blockade suppresses the glutamate induced internalization of GLT-1, both in astrocytes and in a more straightforward experimental system like HEK293 cells transiently transfected with GLT-1. This regulatory mechanism might be relevant to control the amount of GLT-1 transporter at the cell surface in conditions like ischemia or traumatic brain injury, where extracellular concentrations of glutamate are persistently elevated and they promote rapid Ca mobilization.
Versión del editorhttp://dx.doi.org/10.1016/j.neuint.2018.03.012
URIhttp://hdl.handle.net/10261/216971
DOI10.1016/j.neuint.2018.03.012
Identificadoresdoi: 10.1016/j.neuint.2018.03.012
issn: 1872-9754
Aparece en las colecciones: (CBM) Artículos




Ficheros en este ítem:
Fichero Descripción Tamaño Formato
ZafraF_ActivityDependent.pdf1,02 MBAdobe PDFVista previa
Visualizar/Abrir
Mostrar el registro completo

CORE Recommender

SCOPUSTM   
Citations

21
checked on 14-mar-2024

WEB OF SCIENCETM
Citations

19
checked on 28-feb-2024

Page view(s)

121
checked on 19-mar-2024

Download(s)

2.447
checked on 19-mar-2024

Google ScholarTM

Check

Altmetric

Altmetric


NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.