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GABA Withdrawal Syndrome: GABAA receptor, synapse, neurobiological implications and analogies with other abstinences

dc.creatorCalixto, E.
dc.date.accessioned2017-06-29T03:50:17Z
dc.date.available2017-06-29T03:50:17Z
dc.date.issued2016es_ES
dc.identifier2728es_ES
dc.identifier.issn0306-4522es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4577
dc.identifier.urihttps://doi.org/10.1016/j.neuroscience.2015.11.021es_ES
dc.description.abstractes_ES
dc.language.isoenges_ES
dc.publisher[New York?] : Elsevier Sciencees_ES
dc.relation313, 57-72 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshReceptors, GABA-A/metabolismes_ES
dc.subject.meshSubstance Withdrawal Syndrome/metabolismes_ES
dc.subject.meshSynapses/physiologyes_ES
dc.subject.meshgamma-Aminobutyric Acid/deficiencyes_ES
dc.titleGABA Withdrawal Syndrome: GABAA receptor, synapse, neurobiological implications and analogies with other abstinenceses_ES
dc.title.alternativees_ES
dc.typeartículoes_ES
dc.contributor.affiliationDepartamento de Neurobiología, Dirección de Investigaciones en Neurociencias, Instituto Nacional de Psiquiatría ‘‘Ramón de la Fuente”, Calzada México-Xochimilco No. 101, Tlalpan, 14370 México, D.F., Mexicoes_ES
dc.contributor.emailecalixto@imp.edu.mxes_ES
dc.relation.jnabreviadoNEUROSCIENCEes_ES
dc.relation.journalNeurosciencees_ES
dc.identifier.placeEstados Unidoses_ES
dc.date.published2016es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1873-7544es_ES
dc.identifier.doi10.1016/j.neuroscience.2015.11.021es_ES
dc.description.monthEnees_ES
dc.description.abstractotrodiomaAbstract—The sudden interruption of the increase of the concentration of the gamma-aminobutyric acid (GABA), determines an increase in neuronal activity. GABA withdrawal (GW) is a heuristic analogy, with withdrawal symptoms developed by other GABA receptor-agonists such as alcohol, benzodiazepines, and neurosteroids. GW comprises a model of neuronal excitability validated by electroencephalogram (EEG) in which high-frequency and high-amplitude spike–wave complexes appear. In brain slices, GW was identified by increased firing synchronization of pyramidal neurons and by changes in the active properties of the neuronal membrane. GW induces pre- and postsynaptic changes: a decrease in GABA synthesis/release, and the decrease in the expression and composition of GABAA receptors associated with increased calcium entry into the cell. GW is an excellent bioassay for studying partial epilepsy, epilepsy refractory to drug treatment, and a model to reverse or prevent the generation of abstinences from different drugs.es_ES
dc.subject.meshmes_ES
dc.subject.kwes_ES
dc.subject.koGABAes_ES
dc.subject.koNeuronal hyperexcitabilityes_ES
dc.subject.koWithdrawales_ES


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