<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Joglekar R</submitter><funding>NCRR</funding><funding>NIMH</funding><funding>NCATS NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NIEHS</funding><funding>National Institutes of Health</funding><funding>USEPA</funding><pagination>41-54</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8917982</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>89</volume><pubmed_abstract>Nicotine is a neuroteratogenic component of tobacco smoke, e-cigarettes, and other products and can exert sex-specific effects in the developing brain, likely mediated through sex hormones. Estradiol modulates expression of nicotinic acetylcholine receptors in rats, and plays critical roles in neurodevelopmental processes, including sexual differentiation of the brain. Here, we examined the effects of developmental nicotine exposure on the sexual differentiation of the preoptic area (POA), a brain region that normally displays robust structural sexual dimorphisms and controls adult mating behavior in rodents. Using a rat model of gestational exposure, developing pups were exposed to nicotine (2 mg/kg/day) via maternal osmotic minipump (subcutaneously, sc) throughout the critical window for</pubmed_abstract><journal>Neurotoxicology</journal><pubmed_title>Developmental nicotine exposure and masculinization of the rat preoptic area.</pubmed_title><pmcid>PMC8917982</pmcid><funding_grant_id>UL1TR001117</funding_grant_id><funding_grant_id>P01ES022831</funding_grant_id><funding_grant_id>UL1 TR001117</funding_grant_id><funding_grant_id>T32 ES021432</funding_grant_id><funding_grant_id>RD-83543701</funding_grant_id><funding_grant_id>P01 ES022831</funding_grant_id><funding_grant_id>R01 MH052716</funding_grant_id><funding_grant_id>RO1MH52716</funding_grant_id><pubmed_authors>Patisaul HB</pubmed_authors><pubmed_authors>Murphy SK</pubmed_authors><pubmed_authors>Cauley M</pubmed_authors><pubmed_authors>Joglekar R</pubmed_authors><pubmed_authors>Levin ED</pubmed_authors><pubmed_authors>Lipsich T</pubmed_authors><pubmed_authors>Meyer JN</pubmed_authors><pubmed_authors>McCarthy MM</pubmed_authors><pubmed_authors>Corcoran DL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Developmental nicotine exposure and masculinization of the rat preoptic area.</name><description>Nicotine is a neuroteratogenic component of tobacco smoke, e-cigarettes, and other products and can exert sex-specific effects in the developing brain, likely mediated through sex hormones. Estradiol modulates expression of nicotinic acetylcholine receptors in rats, and plays critical roles in neurodevelopmental processes, including sexual differentiation of the brain. Here, we examined the effects of developmental nicotine exposure on the sexual differentiation of the preoptic area (POA), a brain region that normally displays robust structural sexual dimorphisms and controls adult mating behavior in rodents. Using a rat model of gestational exposure, developing pups were exposed to nicotine (2 mg/kg/day) via maternal osmotic minipump (subcutaneously, sc) throughout the critical window for</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-19T07:38:00.864Z</modification><creation>2025-04-19T07:38:00.864Z</creation></dates><accession>S-EPMC8917982</accession><cross_references><pubmed>35026373</pubmed><doi>10.1016/j.neuro.2022.01.005</doi></cross_references></HashMap>