Ver publicación 

Mostrar el registro sencillo de la publicación

Effects of interleukin-1β in glycinergic transmission at the central amygdala

dc.contributor.authorSolorza, Jocelyn
dc.contributor.authorOliva, Carolina A.
dc.contributor.authorCastillo, Karen
dc.contributor.authorAmestica, Gabriela
dc.contributor.authorMaldifassi, María Constanza
dc.contributor.authorLópez-Cortés, Xaviera A.
dc.contributor.authorBarra, Rafael
dc.contributor.authorStehberg, Jimmy
dc.contributor.authorPiesche, Matthias
dc.contributor.authorSáez-Briones, Patricio
dc.contributor.authorGonzález, Wendy
dc.contributor.authorArenas-Salinas, Mauricio
dc.contributor.authorMariqueo, Trinidad A.
dc.date.accessioned2022-01-19T12:28:10Z
dc.date.available2022-01-19T12:28:10Z
dc.date.issued2021
dc.identifier.urihttp://repositorio.ucm.cl/handle/ucm/3736
dc.description.abstractInterleukin-1β (IL-1β) is an important cytokine that modulates peripheral and central pain sensitization at the spinal level. Among its effects, it increases spinal cord excitability by reducing inhibitory Glycinergic and GABAergic neurotransmission. In the brain, IL-1β is released by glial cells in regions associated with pain processing during neuropathic pain. It also has important roles in neuroinflammation and in regulating NMDA receptor activity required for learning and memory. The modulation of glycine-mediated inhibitory activity via IL-1β may play a critical role in the perception of different levels of pain. The central nucleus of the amygdala (CeA) participates in receiving and processing pain information. Interestingly, this nucleus is enriched in the regulatory auxiliary glycine receptor (GlyR) β subunit (βGlyR); however, no studies have evaluated the effect of IL-1β on glycinergic neurotransmission in the brain. Hence, we hypothesized that IL-1β may modulate GlyR-mediated inhibitory activity via interactions with the βGlyR subunit. Our results show that the application of IL-1β (10 ng/ml) to CeA brain slices has a biphasic effect; transiently increases and then reduces sIPSC amplitude of CeA glycinergic currents. Additionally, we performed molecular docking, site-directed mutagenesis, and whole-cell voltage-clamp electrophysiological experiments in HEK cells transfected with GlyRs containing different GlyR subunits. These data indicate that IL-1β modulates GlyR activity by establishing hydrogen bonds with at least one key amino acid residue located in the back of the loop C at the ECD domain of the βGlyR subunit. The present results suggest that IL-1β in the CeA controls glycinergic neurotransmission, possibly via interactions with the βGlyR subunit. This effect could be relevant for understanding how IL-1β released by glia modulates central processing of pain, learning and memory, and is involved in neuroinflammation.es_CL
dc.language.isoenes_CL
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
dc.sourceFrontiers in Pharmacology, 12, 613105es_CL
dc.subjectInterleukin-1βes_CL
dc.subjectAuxiliary subunites_CL
dc.subjectGlycine receptorses_CL
dc.subjectBeta subunites_CL
dc.subjectNeuroimmune communicationes_CL
dc.titleEffects of interleukin-1β in glycinergic transmission at the central amygdalaes_CL
dc.typeArticlees_CL
dc.ucm.facultadFacultad de Medicinaes_CL
dc.ucm.indexacionScopuses_CL
dc.ucm.indexacionIsies_CL
dc.ucm.uriwww.frontiersin.org/articles/10.3389/fphar.2021.613105/fulles_CL
dc.ucm.doidoi.org/10.3389/fphar.2021.613105es_CL


Ficheros en la publicación

FicherosTamañoFormatoVer

No hay ficheros asociados a esta publicación.

Esta publicación aparece en la(s) siguiente(s) colección(ones)

Mostrar el registro sencillo de la publicación

Atribución-NoComercial-SinDerivadas 3.0 Chile
Excepto si se señala otra cosa, la licencia de la publicación se describe como Atribución-NoComercial-SinDerivadas 3.0 Chile