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

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 alteratio...

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Published inSchizophrenia research Vol. 171; no. 1; pp. 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 Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.03.2016
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
MIA
Schizophrenia
GABA
mRNA
Inflammation
GAD
Poly I:C
Online AccessGet full text

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Abstract 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.
AbstractList 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.
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 (GAD 67 ) mRNA expression was examined in male offspring at postnatal day (P)14, P30 and P60. At P60, GAD 67 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.
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.
Author Bronson, Stefanie L
Seroogy, Kim B
Richtand, Neil M
Kyser, Tara L
Hemmerle, Ann M
Ahlbrand, Rebecca
Cassella, Sarah N
Lundgren, Kerstin H
AuthorAffiliation c Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
d San Diego Veterans Affairs Healthcare System, San Diego, CA 92161, USA
a Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
e Department of Psychiatry, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA
b Neuroscience Graduate Program, University of Cincinnati, Cincinnati, OH 45267, USA
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– name: e Department of Psychiatry, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA
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Issue 1
Keywords MIA
Schizophrenia
GABA
mRNA
Inflammation
GAD
Poly I:C
Language English
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Notes Present address for Sarah N. Cassella: Department of Biology, Susquehanna University, Selinsgrove, PA 17870
Present address for Stefanie L. Bronson: Department of Veterinary Animal Biology, University of Pennsylvania, Philadelphia, PA 19104
Both authors contributed equally.
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Snippet Abstract Activation of the maternal innate immune system, termed “maternal immune activation” (MIA), represents a common environmental risk factor for...
Activation of the maternal innate immune system, termed “maternal immune activation” (MIA), represents a common environmental risk factor for schizophrenia....
Activation of the maternal innate immune system, termed "maternal immune activation" (MIA), represents a common environmental risk factor for schizophrenia....
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StartPage 195
SubjectTerms 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
Title Maternal immune activation alters glutamic acid decarboxylase-67 expression in the brains of adult rat offspring
URI https://www.clinicalkey.es/playcontent/1-s2.0-S0920996416300421
https://dx.doi.org/10.1016/j.schres.2016.01.041
https://www.ncbi.nlm.nih.gov/pubmed/26830319
https://pubmed.ncbi.nlm.nih.gov/PMC4803111
Volume 171
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