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

Sarah N Cassella; Ann M Hemmerle; Kerstin H Lundgren; Tara L Kyser; Rebecca Ahlbrand; Stefanie L Bronson; Neil M Richtand; Kim B Seroogy

doi:10.1016/j.schres.2016.01.041

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

Schizophr Res. 2016 Mar;171(1-3):195-9. doi: 10.1016/j.schres.2016.01.041. Epub 2016 Jan 29.

Authors

Sarah N Cassella¹, Ann M Hemmerle², Kerstin H Lundgren², Tara L Kyser¹, Rebecca Ahlbrand³, Stefanie L Bronson⁴, Neil M Richtand⁵, Kim B Seroogy⁶

Affiliations

¹ Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA; Neuroscience Graduate Program, University of Cincinnati, Cincinnati, OH 45267, USA.
² Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
³ Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
⁴ Neuroscience Graduate Program, University of Cincinnati, Cincinnati, OH 45267, USA; Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
⁵ Neuroscience Graduate Program, University of Cincinnati, Cincinnati, OH 45267, USA; Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA; San Diego Veterans Affairs Healthcare System, San Diego, CA 92161, USA; Department of Psychiatry, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA.
⁶ Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA; Neuroscience Graduate Program, University of Cincinnati, Cincinnati, OH 45267, USA. Electronic address: [email protected].

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.

Keywords: GABA; GAD; Inflammation; MIA; Poly I:C; Schizophrenia; mRNA.

Publication types

Research Support, N.I.H., Extramural

MeSH terms

Age Factors
Animals
Animals, Newborn
Autoradiography
Brain / enzymology*
Disease Models, Animal
Female
Gene Expression Regulation, Enzymologic / drug effects
Gene Expression Regulation, Enzymologic / physiology*
Glutamate Decarboxylase / genetics
Glutamate Decarboxylase / metabolism*
Interferon Inducers / toxicity
Male
Poly I-C / toxicity
Pregnancy
Prenatal Exposure Delayed Effects / chemically induced
Prenatal Exposure Delayed Effects / pathology*
RNA, Messenger / metabolism
Rats
Rats, Sprague-Dawley

Substances

Interferon Inducers
RNA, Messenger
Glutamate Decarboxylase
glutamate decarboxylase 1
Poly I-C

Abstract

Publication types

MeSH terms

Substances

Grants and funding