González, L.F.Henríquez-Belmar, F.Delgado-Acevedo, C.Cisternas-Olmedo, M.Arriagada, G.Sotomayor-Zárate, R.Murphy, D.L.Moya, P.R.2018-07-232018-07-232017Biological Research. Volume 50, Issue 1, 19 September 2017, Page 290717-6287DOI: 10.1186/s40659-017-0138-3http://repositorio.unab.cl/xmlui/handle/ria/6346Indexación: Scopus.BACKGROUND: Obsessive-compulsive disorder (OCD) is a severe neuropsychiatric condition affecting 1-3% of the worldwide population. OCD has a strong genetic component, and the SLC1A1 gene that encodes neuronal glutamate transporter EAAT3 is a strong candidate for this disorder. To evaluate the impact of reduced EAAT3 expression in vivo, we studied male EAAT3 heterozygous and wild-type littermate mice using a battery of behavioral paradigms relevant to anxiety (open field test, elevated plus maze) and compulsivity (marble burying), as well as locomotor activity induced by amphetamine. Using high-performance liquid chromatography, we also determined tissue neurotransmitter levels in cortex, striatum and thalamus-brain areas that are relevant to OCD. RESULTS: Compared to wild-type littermates, EAAT3 heterozygous male mice have unaltered baseline anxiety-like, compulsive-like behavior and locomotor activity. Administration of acute amphetamine (5 mg/kg intraperitoneally) increased locomotion with no differences across genotypes. Tissue levels of glutamate, GABA, dopamine and serotonin did not vary between EAAT3 heterozygous and wild-type mice. CONCLUSIONS: Our results indicate that reduced EAAT3 expression does not impact neurotransmitter content in the corticostriatal circuit nor alter anxiety or compulsive-like behaviors.enEAAT3Neuronal glutamate transporterObsessive–compulsive disorderSLC1A1Artículo