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Epidemiological and experimental data indicate that maternal infections are a significant and preventable cause of preterm birth. Recently, melatonin has been suggested to exert neuroprotective effects in several models of brain injury. Here, we sought to investigate whether the administration of melatonin is able to prevent lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>)\u2010induced fetal brain damage in a model of <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced preterm labor. For this purpose, 15\u2010day pregnant <jats:styled-content style=\"fixed-case\">BALB<\/jats:styled-content>\/c mice received intraperitoneally 2 doses of <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> or vehicle: the first one at 10:00\u00a0hours (0.26\u00a0mg\/kg) and the second at 13:00\u00a0hours (0.52\u00a0mg\/kg). On day 14 of pregnancy, a group of mice was subcutaneously implanted with a pellet of 25\u00a0mg melatonin. This experimental protocol resulted in 100% of preterm birth and pup death in the <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> group and a 50% of term birth and pup survival in the melatonin\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> group. In the absence of melatonin, fetuses from <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010treated mothers showed histological signs of brain damage, microglial\/macrophage activation, and higher levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2, inducible nitric oxide synthase (NOS), and neuronal NOS <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>s as well as increased histone acetyltransferase activity and histone H3 hyperacetylation. In contrast, antenatal administration of melatonin prevented <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced fetal brain damage. Moreover, when behavioral traits were analyzed in the offspring from control, melatonin, and melatonin\u00a0+\u00a0<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>, no significant differences were found, suggesting that melatonin prevented <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced long\u2010term neurodevelopmental impairments. Collectively, our results suggest that melatonin could be a new therapeutic tool to prevent fetal brain damage and its long\u2010term consequences induced by maternal inflammation.<\/jats:p>","DOI":"10.1111\/jpi.12439","type":"journal-article","created":{"date-parts":[[2017,8,4]],"date-time":"2017-08-04T11:12:48Z","timestamp":1501845168000},"source":"Crossref","is-referenced-by-count":37,"title":["Maternal administration of melatonin exerts short\u2010 and long\u2010term neuroprotective effects on the offspring from lipopolysaccharide\u2010treated mice"],"prefix":"10.1111","volume":"63","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4499-8397","authenticated-orcid":false,"given":"Ana Paula","family":"Dom\u00ednguez Rubio","sequence":"first","affiliation":[{"name":"Laboratorio de Fisiopatolog\u00eda de la Pre\u00f1ez y el Parto Facultad de Medicina Centro de Estudios Farmacol\u00f3gicos y Bot\u00e1nicos (CEFyBO) Consejo Nacional de Investigaciones Cient\u00edficas y T\u00e9cnicas 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