Prenatal immune activation and subsequent peripubertal stress as a new model of schizophrenia

Abstract

Evaluation of: Giovanoli S, Engler H, Engler A et al. Stress in puberty unmasks latent neuropathological consequences of prenatal immune activation in mice. Science 339(6123), 1095–1099 (2013).

Epidemiological studies show that maternal viral infection during pregnancy plays a key role in the etiology of neurodevelopmental disorders, such as schizophrenia and autism. Prenatal maternal immune activation and peripubertal psychological stress are key environmental risk factors for neurodevelopmental disorders. Viral mimic polyriboinosinic-polyribocytidylic acid is known to act as a Toll-like receptor-3 agonist. Polyriboinosinic-polyribocytidylic acid has been typically used to establish this rodent model of prenatal immune activation. Recently, Giovanoli et al. reported on a new neurodevelopmental model of schizophrenia based on combined prenatal immune activation and peripubertal stress. In this report, we place these findings into context and discuss their significance.

Keywords::

• auditory sensory gating
• dopamine
• microglial activation
• peripubertal stress
• prenatal immune activation
• schizophrenia
• two-hit model

Financial & competing interests disclosure

This study was supported by a Grant-in-Aid for Scientific Research on Innovative Areas of the Ministry of Education, Culture, Sports, Science and Technology, Japan (K Hashimoto). N Yoshimi and T Futamura are employers of Otsuka Pharmaceutical Co., Ltd. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript.

No writing assistance was utilized in the production of this manuscript.