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This becomes most evident in untreated congenital hypothyroidism, leading to irreversible mental retardation. Likewise, maternal hypothyroxinaemia, a lack of <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> during pregnancy, is associated with neurological dysfunction in the offspring, such as autism and reduced intellectual capacity. In the brain, <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> acts mainly through <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> receptor \u03b11 (<jats:styled-content style=\"fixed-case\">TR\u03b1<\/jats:styled-content>1). Consequently, mice heterozygous for a dominant\u2010negative mutation in <jats:styled-content style=\"fixed-case\">TR\u03b11<\/jats:styled-content> display profound neuroanatomical abnormalities including deranged development of parvalbumin neurones. However, the exact timing and orchestration of <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> signalling during parvalbumin neurone development remains elusive. In the present study, we dissect the development of parvalbumin neurones in the anterior hypothalamic area (<jats:styled-content style=\"fixed-case\">AHA<\/jats:styled-content>) in male mice using different mouse models with impaired pre\u2010 and postnatal <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> signalling in combination with bromodeoxyuridine birth dating and immunohistochemistry. Our data reveal that hypothalamic parvalbumin neurones are born at embryonic day 12 and are first detected in the <jats:styled-content style=\"fixed-case\">AHA<\/jats:styled-content> at postnatal day 8, reaching their full population number at P13. Interestingly, they do not require <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> postnatally because their development is not impaired in mice with impaired <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> signalling after birth. By contrast, however, these neurones crucially depend on <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> through <jats:styled-content style=\"fixed-case\">TR\u03b1<\/jats:styled-content>1 signalling in the second half of pregnancy, when the hormone is almost exclusively provided by the mother. For the first time, our findings directly link a maternal hormone to a neuroanatomical substrate in the foetal brain, and underline the importance of proper <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> signalling during pregnancy for offspring mental health. Given the role of hypothalamic parvalbumin neurones in the central control of blood pressure, the present study advocates the inclusion of cardiovascular parameters in the current discussion on possible <jats:styled-content style=\"fixed-case\">TH<\/jats:styled-content> substitution in maternal hypothyroxinaemia.<\/jats:p>","DOI":"10.1111\/jne.12573","type":"journal-article","created":{"date-parts":[[2018,1,29]],"date-time":"2018-01-29T22:19:20Z","timestamp":1517264360000},"source":"Crossref","is-referenced-by-count":34,"title":["Maternal thyroid hormone is required for parvalbumin neurone development in the anterior hypothalamic area"],"prefix":"10.1111","volume":"30","author":[{"given":"L.","family":"Harder","sequence":"first","affiliation":[{"name":"Center of Brain, Behavior and Metabolism CBBM\/Medizinische Klinik I University of L\u00fcbeck  L\u00fcbeck 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