RESUMEN

Environmental risk factors that operate at foetal or neonatal levels increase the vulnerability to schizophrenia, plausibly via stress-immune activation that perturbs the epidermal growth factor (EGF) system, a system critical for neurodevelopment. We investigated potential associations between environmental insults and immune and EGF system changes through a maternal immune activation (MIA) model, using the precocial spiny mice (Acomys cahirinus). After mid-gestation MIA prepubescent offspring showed elevated NF-κB1 protein in nucleus accumbens, decreased EGFR in caudate putamen and a trend for increased PI3K-110δ in ventral hippocampus. Thus, prenatal stress may cause a heightened NF-κB1-mediated immune attenuation of EGF system signalling.

Asunto(s)

Conducta Animal/fisiología , Encéfalo/metabolismo , Factor de Crecimiento Epidérmico/sangre , FN-kappa B/sangre , Efectos Tardíos de la Exposición Prenatal/inmunología , Esquizofrenia/inmunología , Animales , Biomarcadores/sangre , Modelos Animales de Enfermedad , Femenino , Genes erbB-1 , Hipocampo/metabolismo , Ratones , Actividad Motora/efectos de los fármacos , Neuritas/metabolismo , Embarazo , Esquizofrenia/etiología , Esquizofrenia/metabolismo , Transducción de Señal