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Human evidence of altered female pubertal timing after exposure to endocrine disrupting chemicals (<jats:styled-content style=\"fixed-case\">EDC<\/jats:styled-content>s) is equivocal. Among the limiting factors, most studies evaluate exposure to single <jats:styled-content style=\"fixed-case\">EDC<\/jats:styled-content>s at the time of puberty and hardly assess the impact of lifelong exposure to mixtures of <jats:styled-content style=\"fixed-case\">EDC<\/jats:styled-content>s. Some rodent and ovine studies indicate a possible role of foetal and neonatal exposure to <jats:styled-content style=\"fixed-case\">EDC<\/jats:styled-content>s, in accordance with the concept of an early origin of health and disease. Such effects possibly involve neuroendocrine mechanisms because the hypothalamus is a site where homeostasis of reproduction, as well as control of energy balance, is programmed and regulated. In our previous studies, pulsatile <jats:styled-content style=\"fixed-case\">g<\/jats:styled-content>onadotrophin\u2010<jats:styled-content style=\"fixed-case\">r<\/jats:styled-content>eleasing <jats:styled-content style=\"fixed-case\">h<\/jats:styled-content>ormone (<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>n<jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content>) secretion control via oestrogen, glutamate and aryl hydrocarbon receptors was shown to be involved in the mechanism of sexual precocity after early postnatal exposure to the insecticide dichlorodiphenyltrichloroethane. Very recently, we have shown that neonatal exposure to the potent synthetic oestrogen diethylstilbestrol (<jats:styled-content style=\"fixed-case\">DES<\/jats:styled-content>) is followed by early or delayed puberty depending on the dose, with consistent changes in developmental increase of <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>n<jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content> pulse frequency. Moreover, <jats:styled-content style=\"fixed-case\">DES<\/jats:styled-content> results in reduced leptin stimulation of <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>n<jats:styled-content style=\"fixed-case\">RH<\/jats:styled-content> secretion <jats:italic>in vitro<\/jats:italic>, an effect that is additive with prenatal food restriction. Thus, using puberty as an endpoint of the effects of <jats:styled-content style=\"fixed-case\">EDC<\/jats:styled-content>, it appears necessary to consider pre\u2010 and perinatal exposure to low doses and to pay attention to the other conditions of prenatal life, such as energy availability, keeping in mind the possibility that puberty could not only be advanced, but also delayed through neuroendocrine mechanisms.<\/jats:p>","DOI":"10.1111\/jne.12107","type":"journal-article","created":{"date-parts":[[2013,9,12]],"date-time":"2013-09-12T15:37:09Z","timestamp":1379000229000},"page":"1079-1087","source":"Crossref","is-referenced-by-count":34,"title":["Early Neuroendocrine Disruption in Hypothalamus and Hippocampus: Developmental Effects Including Female Sexual Maturation and Implications for Endocrine Disrupting Chemical Screening"],"prefix":"10.1111","volume":"25","author":[{"given":"J.\u2010P.","family":"Bourguignon","sequence":"first","affiliation":[{"name":"Developmental 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