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Although rodent models of hypoxia have been reported, the detailed pathogenesis of maternal hypoxia\u2010induced neurodevelopmental disorders remains unclear. The objectives of this study are to understand the pathophysiological mechanisms underlying maternal hypoxia\u2010related neurodevelopmental disorders and to identify new drug targets for these pathologies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>A newly generated rat model exhibiting maternal hypoxia\u2010induced neurodevelopmental disorder\u2010like phenotypes was employed for behavioural assessments. Immunohistochemical analysis was performed on foetal and adult rat brain sections to characterise structural alterations. Furthermore, synaptic transmission and microstructural changes resulting from maternal hypoxia were examined utilising extracellular electrophysiological recordings and transmission electron microscopy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      A rat model of maternal hypoxia\u2010induced neurodevelopmental disorders was established. Immunohistochemical analysis showed a reduction in the density of excitatory pyramidal neurones in layer II\/III of the anterior cingulate cortex. Moreover, excitatory neurogenesis was disrupted following gestational exposure to hypoxia. Extracellular electrophysiological recordings in the anterior cingulate cortex region demonstrated decreased synaptic responsiveness, potentially attributable to a reduction in presynaptic vesicle density. Remarkably, pharmacological antagonism of mGlu\n                      <jats:sub>2\/3<\/jats:sub>\n                      receptors with LY341495 abolished the neurodevelopmental disorder\u2010like phenotypes in the experimental animals.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and Implications<\/jats:title>\n                    <jats:p>Maternal hypoxia\u2010induced neurodevelopmental disorder\u2010like behaviours point to morphological and\/or functional deficits in excitatory pyramidal neurones, potentially causing excitatory\/inhibitory imbalance in the anterior cingulate cortex. Enhancing excitatory synaptic response may represent a novel therapeutic strategy for hypoxia\u2010related neurodevelopmental disorders.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70435","type":"journal-article","created":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T11:36:56Z","timestamp":1775648216000},"page":"3723-3742","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["In rats, neurodevelopmental disorders induced by maternal hypoxia are associated with attenuated excitatory neurotransmission in the cingulate cortex"],"prefix":"10.1111","volume":"183","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8478-5885","authenticated-orcid":false,"given":"Kentaro","family":"Tokudome","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Graduate School of Medicine Osaka Metropolitan University  Osaka Japan"},{"name":"Division of Glocal Pharmacology, Department of Pharmacology, 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