Maternal immune activation alters glutamic acid decarboxylase-67 expression in the brains of adult rat offspring

• Published in: Schizophrenia research 2016-03, Vol.171 (1), p.195-199
• Main Authors: Cassella, Sarah N, Hemmerle, Ann M, Lundgren, Kerstin H, Kyser, Tara L, Ahlbrand, Rebecca, Bronson, Stefanie L, Richtand, Neil M, Seroogy, Kim B
• Format: Article
• Language: English
• Subjects: Age Factors; Animals; Animals, Newborn; Autoradiography; Brain - enzymology; Disease Models, Animal; Female; GABA; GAD; Gene Expression Regulation, Enzymologic - drug effects; Gene Expression Regulation, Enzymologic - physiology; Glutamate Decarboxylase - genetics; Glutamate Decarboxylase - metabolism; Inflammation; Interferon Inducers - toxicity; Male; MIA; mRNA; Poly I-C - toxicity; Poly I:C; Pregnancy; Prenatal Exposure Delayed Effects - chemically induced; Prenatal Exposure Delayed Effects - pathology; Psychiatry; Rats; Rats, Sprague-Dawley; RNA, Messenger - metabolism; Schizophrenia
• ISSN: 0920-9964; 1573-2509
• DOI: 10.1016/j.schres.2016.01.041

Abstract Activation of the maternal innate immune system, termed “maternal immune activation” (MIA), represents a common environmental risk factor for schizophrenia. Whereas evidence suggests dysregulation of GABA systems may underlie the pathophysiology of schizophrenia, a role for MIA in alteration of GABAergic systems is less clear. Here, pregnant rats received either the viral mimetic polyriboinosinic–polyribocytidilic acid or vehicle injection on gestational day 14. Glutamic acid decarboxylase-67 (GAD67 ) mRNA expression was examined in male offspring at postnatal day (P)14, P30 and P60. At P60, GAD67 mRNA was elevated in hippocampus and thalamus and decreased in prefrontal cortex of MIA offspring. MIA-induced alterations in GAD expression could contribute to the pathophysiology of schizophrenia.