dc.creatorLorca-Ponce, Enrique
dc.creatorLara-Suzarte, Marcelo Andrés
dc.creatorLoyola, S
dc.creatorPino, D
dc.creatorRojas-Montecinos, Patricio Alejandro
dc.date2018-09-21T12:13:54Z
dc.date2022-06-18T19:25:07Z
dc.date2018-09-21T12:13:54Z
dc.date2022-06-18T19:25:07Z
dc.date2013-10-04
dc.date2013
dc.date2013-10-01
dc.date.accessioned2023-08-21T21:44:46Z
dc.date.available2023-08-21T21:44:46Z
dc.identifier1130904
dc.identifierhttps://hdl.handle.net/10533/220593
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8286195
dc.descriptionSchizophrenia is one of the most common neurological diseases in human population, however there is no common hypothesis to explaining all its features. This is due in part to a inability of animal models to reproduce all the features observed in human patients. In this work we use Ketamine administration to generate a schizophrenia and psychosis-like animal model. Adult animals (7 weeks old) were injected intraperitoneally with of Ketamine (30 mgr/kgr) for five days. After two days locomotor activity showed to be significative higher than in control animals, as showed in other animal models. Because Hippocampus is one of the brain regions that showed alteration in this disease, Extracellular field recordings of the CA3-CA1 synapse were performed to evaluate the circuit excitability. In addition, Ketamine treated animals showed a decrease in the Input-Output relationship of Excitatory Post Synaptic Potentials (EPSP). In order to test the hypothesis that a decrease in inhibition can explain part of this pathology, we are assaying the function of the chloride co-transporter NKCC1, which modifies the excitation to inhibition balance due to GABA release. In summary, we validated the ketamine model by using both behavioral and electrophysiological methods and propose its usefullnes for studied of schizophrenia and psichosis-like disorders.
dc.languageeng
dc.relationinstname: Conicyt
dc.relationreponame: Repositorio Digital RI2.0
dc.relationReunión Anual Sociedad Chilena de Neurociencias
dc.relation9
dc.relationinfo:eu-repo/grantAgreement//1130904
dc.relationinfo:eu-repo/semantics/dataset/hdl.handle.net/10533/93486
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.titleChloride transporte NKCC1 involvment in reduced excitability in an animal model of schizophrenia
dc.typePonencia
dc.typeinfo:eu-repo/semantics/lecture
dc.coverageValparaíso


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