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dc.creatorVillalobos, Nelsones_ES
dc.creatorAlmazán-Alvarado, Salvadores_ES
dc.creatorMagdaleno-Madrigal, Victor Manueles_ES
dc.date2022
dc.date.accessioned2025-01-09T20:26:57Z
dc.date.available2025-01-09T20:26:57Z
dc.date.issued2022
dc.identifierJC39NC22es_ES
dc.identifier.issn1880-6546
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/8193
dc.identifier.urihttps://doi.org/10.1186/s12576-022-00843-3
dc.descriptionThe external globus pallidus (GP) is a GABAergic node involved in motor control regulation and coordinates firing and synchronization in the basal ganglia-thalamic-cortical network through inputs and electrical activity. In Parkinson's disease, high GABA levels alter electrical activity in the GP and contribute to motor symptoms. Under normal conditions, GABA levels are regulated by GABA transporters (GATs). GAT type 1 (GAT-1) is highly expressed in the GP, and pharmacological blockade of GAT-1 increases the duration of currents mediated by GABA A receptors and induces tonic inhibition. The functional contribution of the pathway between the GP and the reticular thalamic nucleus (RTn) is unknown. This pathway is important since the RTn controls the flow of information between the thalamus and cortex, suggesting that it contributes to cortical dynamics. In this work, we investigated the effect of increased GABA levels on electrical activity in the RTn by obtaining single-unit extracellular recordings from anesthetized rats and on the motor cortex (MCx) by corticography. Our results show that high GABA levels increase the spontaneous activity rate of RTn neurons and desynchronize oscillations in the beta frequency band in the MCx. Our findings provide evidence that the GP exerts tonic control over RTn activity through the GP-reticular pathway and functionally contributes to cortical oscillation dynamics.es_ES
dc.formatPDFes_ES
dc.language.isoenges_ES
dc.publisherSpringer Japanes_ES
dc.relation72(1):17
dc.rightsAcceso Cerradoes_ES
dc.titleElevation of GABA levels in the globus pallidus disinhibits the thalamic reticular nucleus and desynchronized cortical beta oscillationses_ES
dc.typeArtículoes_ES
dc.contributor.affiliationAcademia de Fisiología, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Colonia Casco de Santo Tomás, 11340, Ciudad de México, Mexico
dc.contributor.emailnvillalobosv@ipn.mx; maleno@imp.edu.mx ; malenomad@gmail.com
dc.relation.jnabreviadoJ PHYSIOL SCI
dc.relation.journalJournal of Physiological Sciences
dc.identifier.placeJapón
dc.date.published2022
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz
dc.identifier.eissn1880-6562
dc.identifier.doi10.1186/s12576-022-00843-3
dc.subject.kwMotor control
dc.subject.kwGlobus pallidus
dc.subject.kwBeta band
dc.subject.kwTonic inhibition
dc.subject.kwReticular thalamic nucleus
dc.subject.kwSynchronization


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