The Opening of Connexin 43 Hemichannels Alters Hippocampal Astrocyte Function and Neuronal Survival in Prenatally LPS-Exposed Adult Offspring

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dc.catalogadorjlo
dc.contributor.authorChávez Chaname, Carolina Elizabeth
dc.contributor.authorOyarzún Isamitt, Juan Esteban
dc.contributor.authorAvendaño, Beatriz C.
dc.contributor.authorMellado, Luis A.
dc.contributor.authorInostroza, Carla A.
dc.contributor.authorAlvear Soto, Tanhia Francheska
dc.contributor.authorOrellana Roca, Juan Andrés
dc.date.accessioned2024-10-15T19:35:14Z
dc.date.available2024-10-15T19:35:14Z
dc.date.issued2019
dc.description.abstractClinical evidence has revealed that children born from mothers exposed to viral and bacterial pathogens during pregnancy are more likely to suffer various neurological disorders including schizophrenia, autism bipolar disorder, major depression, epilepsy, and cerebral palsy. Despite that most research has centered on the impact of prenatal inflammation in neurons and microglia, the potential modifications of astrocytes and neuron-astrocyte communication have received less scrutiny. Here, we evaluated whether prenatally LPS-exposed offspring display alterations in the opening of astrocyte hemichannels and pannexons in the hippocampus, together with changes in neuroinflammation, intracellular Ca2+ and nitric oxide (NO) signaling, gliotransmitter release, cell arborization, and neuronal survival. Ethidium uptake recordings revealed that prenatal LPS exposure enhances the opening of astrocyte Cx43 hemichannels and Panx1 channels in the hippocampus of adult offspring mice. This enhanced channel activity occurred by a mechanism involving a microglia-dependent production of IL-1 beta/TNF-alpha and the stimulation of p38 MAP kinase/iNOS/[Ca2+](i)-mediated signaling and purinergic/glutamatergic pathways. Noteworthy, the activity of Cx43 hemichannels affected the release of glutamate, [Ca2+](i) handling, and morphology of astrocytes, whereas also disturbed neuronal function, including the dendritic arbor and spine density, as well as survival. We speculate that excitotoxic levels of glutamate triggered by the activation of Cx43 hemichannels may contribute to hippocampal neurotoxicity and damage in prenatally LPS-exposed offspring. Therefore, the understanding of how astrocyte-neuron crosstalk is an auspicious avenue toward the development of broad treatments for several neurological disorders observed in children born to women who had a severe infection during gestation.
dc.fechaingreso.objetodigital2024-10-15
dc.format.extent19 páginas
dc.fuente.origenConveris
dc.identifier.doi10.3389/fncel.2019.00460
dc.identifier.issn1662-5102
dc.identifier.pubmedidMEDLINE:31680871
dc.identifier.scopusid2-s2.0-85074139290
dc.identifier.urihttps://doi.org/10.3389/fncel.2019.00460
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/88238
dc.identifier.wosidWOS:000497804800001
dc.information.autorucFacultad de Ciencias Biológicas; Chávez Chaname, Carolina Elizabeth; S/I; 179033
dc.information.autorucEscuela de Medicina; Oyarzún Isamitt, Juan Esteban; 0000-0002-9695-7207; 171970
dc.information.autorucEscuela de Medicina; Alvear Soto, Tanhia Francheska; 0009-0007-8691-4901; 1246198
dc.information.autorucEscuela de Medicina; Orellana Roca, Juan Andrés; 0000-0003-4076-207X; 126007
dc.language.isoen
dc.nota.accesocontenido completo
dc.pagina.final19
dc.pagina.inicio1
dc.revistaFrontiers In Cellular Neuroscience
dc.rightsacceso abierto
dc.subjectNeuroinflammation
dc.subjectHemichannel
dc.subjectConnexin
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.titleThe Opening of Connexin 43 Hemichannels Alters Hippocampal Astrocyte Function and Neuronal Survival in Prenatally LPS-Exposed Adult Offspring
dc.typeartículo
dc.volumen13
sipa.codpersvinculados179033
sipa.codpersvinculados171970
sipa.codpersvinculados1246198
sipa.codpersvinculados126007
sipa.trazabilidadConveris;20-07-2021
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