Increased Levels of C1q in the Prefrontal Cortex of Adult Offspring after Maternal Immune Activation: Prevention by 7,8-Dihydroxyflavone.
- Author:
Mei HAN
1
;
Ji Chun ZHANG
;
Kenji HASHIMOTO
Author Information
- Publication Type:Original Article
- Keywords: Brain-derived neurotrophic factor; Complement protein C1q; Maternal immune activation; Prefrontal cortex; TrkB
- MeSH: Adolescent; Adult Children*; Adult*; Animals; Blotting, Western; Brain; Brain-Derived Neurotrophic Factor; Complement System Proteins; Frontal Lobe; Humans; Mice; Phosphotransferases; Prefrontal Cortex*; Prodromal Symptoms; Psychotic Disorders; Schizophrenia; Tropomyosin
- From:Clinical Psychopharmacology and Neuroscience 2017;15(1):64-67
- CountryRepublic of Korea
- Language:English
- Abstract: OBJECTIVE: Prenatal infection is implicated in the etiology of schizophrenia. The objective of this paper is to study the role of complement protein C1q in the psychosis of adult offspring after maternal immune activation (MIA). In addition, effect of 7,8-dihydroxyflavone (7,8-DHF: a tropomyosin receptor kinase B [TrkB] agonist) was also examined. METHODS: Western blot analysis of C1q in the brain regions from adult offspring after prenatal poly(I:C) (5.0 mg/kg/day from E12 to E17) exposure was performed. 7,8-DHF or vehicle was given from 4 to 8-weeks old. RESULTS: Expression of C1q in the prefrontal cortex (PFC) of adult offspring from poly(I:C)-treated pregnant mice was significantly higher than that of control group. Early treatment with 7,8-DHF during juvenile and adolescent stages could prevent an increase of C1q in the PFC of adult offspring after MIA. CONCLUSION: Therefore, it is likely that increased C1q expression in the frontal cortex may play a role in the behavioral abnormalities of adult offspring after MIA. Furthermore, supplementation with a TrkB agonist such as 7,8-DHF during the prodromal stage may have prophylactic effects on the behavioral abnormalities after MIA.
