Development
Author: Facundo Mateo Martin | Email: facundo.martin@unc.edu.ar
Facundo Mateo Martin1°2°3°, Estela Maris Muñoz4°, Agata Rita Carpentieri1°3°, Maria Elena Peralta Lopez1°2°
1° Cátedra B de Química Biológica-Facultad de Odontología-UNC, Córdoba, Argentina
2° Cátedra de Bioquímica y Biología Molecular FCM-UNC, Córdoba, Argentina
3° INICSA-UNC-CONICET, Córdoba, Argentina
4° Laboratorio de Neurobiología Básica y Traslacional, IHEM-UNCuyo-CONICET, Mendoza, Argentina.
Schizophrenia, a mental disorder with unclear etiophysiopathology, presents with delirium, hallucinations, social isolation and cognitive alterations. There are various animal models of schizophrenia. The first and most widely studied are based on alterations in different neurotransmission systems. Recently, maternal immune activation (MIA) by infectious conditions during pregnancy has begun to be studied. These insults can trigger persistent neuroinflammation in the offspring, impair neurodevelopment and cause a schizophrenia-like syndrome. In the present work we set out to establish and characterize a model of MIA in Wistar rats induced by poly I:C acid IP on day 12 of gestation. Systemic parameters and acute phase inflammatory reactive parameters were analyzed in blood obtained by cardiac puncture 24 hours after the injection of poly I:C in doses of 5, 10 and 20 mg/kg body weight. No significant differences were detected in blood count, C reative protein (CRP) and ultrasensitive CRP of the rats treated with poly I:C acid and the controls. Body temperature was similar in both groups. The analysis of proinflammatory interleukins would be important to confirm systemic inflammation capable of determining neuroinflammation in the offspring. We are processing other inflammatory and behavioral parameters in the MIA offspring that could confirm this as a model of schizophrenia.