<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gumusoglu, S. B.</style></author><author><style face="normal" font="default" size="100%">Stevens, H. E.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Maternal Inflammation and Neurodevelopmental Programming: A Review of Preclinical Outcomes and Implications for Translational Psychiatry</style></title><secondary-title><style face="normal" font="default" size="100%">Biol Psychiatry</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Biological psychiatry</style></alt-title><short-title><style face="normal" font="default" size="100%">Biological psychiatryBiological psychiatry</style></short-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animal model</style></keyword><keyword><style  face="normal" font="default" size="100%">Behavioral neuroscience</style></keyword><keyword><style  face="normal" font="default" size="100%">Maternal immune activation</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular and cellular psychiatry</style></keyword><keyword><style  face="normal" font="default" size="100%">neurodevelopment</style></keyword><keyword><style  face="normal" font="default" size="100%">Prenatal inflammation</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jan 15</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">2</style></number><edition><style face="normal" font="default" size="100%">2018/10/16</style></edition><volume><style face="normal" font="default" size="100%">85</style></volume><pages><style face="normal" font="default" size="100%">107-121</style></pages><isbn><style face="normal" font="default" size="100%">0006-3223</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Early disruptions to neurodevelopment are highly relevant to understanding both psychiatric risk and underlying pathophysiology that can be targeted by new treatments. Much convergent evidence from the human literature associates inflammation during pregnancy with later neuropsychiatric disorders in offspring. Preclinical models of prenatal inflammation have been developed to examine the causal maternal physiological and offspring neural mechanisms underlying these findings. Here we review the strengths and limitations of preclinical models used for these purposes and describe selected studies that have shown maternal immune impacts on the brain and behavior of offspring. Maternal immune activation in mice, rats, nonhuman primates, and other mammalian model species have demonstrated convergent outcomes across methodologies. These outcomes include shifts and/or disruptions in the normal developmental trajectory of molecular and cellular processes in the offspring brain. Prenatal developmental origins are critical to a mechanistic understanding of maternal immune activation-induced alterations to microglia and immune molecules, brain growth and development, synaptic morphology and physiology, and anxiety- and depression-like, sensorimotor, and social behaviors. These phenotypes are relevant to brain functioning across domains and to anxiety and mood disorders, schizophrenia, and autism spectrum disorder, in which they have been identified. By turning a neurodevelopmental lens on this body of work, we emphasize the importance of acute changes to the prenatal offspring brain in fostering a better understanding of potential mechanisms for intervention. Collectively, overlapping results across maternal immune activation studies also highlight the need to examine preclinical offspring neurodevelopment alterations in terms of a multifactorial immune milieu, or immunome, to determine potential mechanisms of psychiatric risk.</style></abstract><accession-num><style face="normal" font="default" size="100%">30318336</style></accession-num><notes><style face="normal" font="default" size="100%">1873-2402&lt;br/&gt;Gumusoglu, Serena B&lt;br/&gt;Stevens, Hanna E&lt;br/&gt;P30 ES005605/ES/NIEHS NIH HHS/United States&lt;br/&gt;Journal Article&lt;br/&gt;Review&lt;br/&gt;United States&lt;br/&gt;Biol Psychiatry. 2019 Jan 15;85(2):107-121. doi: 10.1016/j.biopsych.2018.08.008. Epub 2018 Aug 27.</style></notes><auth-address><style face="normal" font="default" size="100%">Interdisciplinary Graduate Program in Neuroscience, University of Iowa, Iowa City, Iowa.&lt;br/&gt;Interdisciplinary Graduate Program in Neuroscience, University of Iowa, Iowa City, Iowa; Department of Psychiatry, Carver College of Medicine, University of Iowa, Iowa City, Iowa; Iowa Neuroscience Institute, University of Iowa, Iowa City, Iowa. Electronic address: hanna-stevens@uiowa.edu.</style></auth-address><remote-database-provider><style face="normal" font="default" size="100%">NLM</style></remote-database-provider></record></records></xml>