Prolonged activation of NMDA receptors promotes dephosphorylation and alters postendocytic sorting of GABAB receptors
Author
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Terunuma, Miho
Author
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Vargas, Karina J.
Author
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Wilkins, Megan E.
Author
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Ramírez, Omar A.
Author
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Jaureguiberry-Bravo, Matías
Author
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Pangalos, Menelas N.
Author
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Smart, Trevor G.
Author
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Moss, Stephen J.
Author
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Couve, Andrés
Admission date
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2019-03-11T13:00:14Z
Available date
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2019-03-11T13:00:14Z
Publication date
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2010
Cita de ítem
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Proceedings of the National Academy of Sciences of the United States of America, Volumen 107, Issue 31, 2018, Pages 13918-13923
Identifier
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00278424
Identifier
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10916490
Identifier
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10.1073/pnas.1000853107
Identifier
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https://repositorio.uchile.cl/handle/2250/165069
Abstract
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Slow and persistent synaptic inhibition is mediated by metabotropic GABAB receptors (GABABRs). GABABRs are responsible for the modulation of neurotransmitter release from presynaptic terminals and for hyperpolarization at postsynaptic sites. Postsynaptic GABABRs are predominantly found on dendritic spines, adjacent to excitatory synapses, but the control of their plasma membrane availability is still controversial. Here, we explore the role of glutamate receptor activation in regulating the function and surface availability of GABABRs in central neurons. We demonstrate that prolonged activation of NMDA receptors (NMDA-Rs) leads to endocytosis, a diversion from a recycling route, and subsequent lysosomal degradation of GABABRs. These sorting events are paralleled by a reduction in GABABR-dependent activation of inwardly rectifying K+ channel currents. Postendocytic sorting is critically dependent on phosphorylation of serine 783 (S783) within the GABABR2 subunit, an established substrat