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Developmental Nicotine Exposure Indu...
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Buck, Jordan Matthew.
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Developmental Nicotine Exposure Induces Intergenerational Transmission of an Ensemble of Neurodevelopmental Disorder-Like Behavioral, Neuropharmacological, Neurotrophic, Neuroendocrine, Epigenetic, and Neurotranscriptomic Phenotypes in Adolescent Mice.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Developmental Nicotine Exposure Induces Intergenerational Transmission of an Ensemble of Neurodevelopmental Disorder-Like Behavioral, Neuropharmacological, Neurotrophic, Neuroendocrine, Epigenetic, and Neurotranscriptomic Phenotypes in Adolescent Mice./
作者:
Buck, Jordan Matthew.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2020,
面頁冊數:
232 p.
附註:
Source: Dissertations Abstracts International, Volume: 81-11.
Contained By:
Dissertations Abstracts International81-11.
標題:
Neurosciences. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=27833587
ISBN:
9798645451677
Developmental Nicotine Exposure Induces Intergenerational Transmission of an Ensemble of Neurodevelopmental Disorder-Like Behavioral, Neuropharmacological, Neurotrophic, Neuroendocrine, Epigenetic, and Neurotranscriptomic Phenotypes in Adolescent Mice.
Buck, Jordan Matthew.
Developmental Nicotine Exposure Induces Intergenerational Transmission of an Ensemble of Neurodevelopmental Disorder-Like Behavioral, Neuropharmacological, Neurotrophic, Neuroendocrine, Epigenetic, and Neurotranscriptomic Phenotypes in Adolescent Mice.
- Ann Arbor : ProQuest Dissertations & Theses, 2020 - 232 p.
Source: Dissertations Abstracts International, Volume: 81-11.
Thesis (Ph.D.)--University of Colorado at Boulder, 2020.
This item must not be sold to any third party vendors.
Smoking during pregnancy confers liability to neurodevelopmental disorders such as ADHD, autism, and schizophrenia in children and potentially grandchildren as well. Modeling the intergenerationally transmissible phenotypic consequences of smoking during pregnancy, the experiments embodying this thesis examined the behavioral, neuropharmacological, neurobiological, epigenetic, and neurotranscriptomic impacts of developmental nicotine exposure in the adolescent offspring and grandoffspring of nicotine-exposed female mice. Results demonstrate that developmental nicotine exposure elicits multigenerational hyperactivity and risk-taking behaviors, aberrant circadian rhythmicity of activity, enhanced nicotine intake, therapeutic-like behavioral responsivity to methylphenidate and nicotine, corticostriatothalamic nicotinic acetylcholine receptor dysfunction, corticostriatal dopamine transporter dysfunction, impaired corticostriatal proBDNF proteolysis which correlates with furin deficits, corticostriatal glucocorticoid receptor hypoactivity, hypocorticosteronemia, corticostriatal DNA methylome and DNA methyltransferase 3A deficits, downregulation of methyl-CpG-binding protein 2 and histone deacetylase 2 in the frontal cortices and hippocampi, and an array of transcriptomic anomalies in dopamine receptor D1-expressing striatal medium spiny neurons. This phenotypic ensemble recapitulates behavioral, neuropharmacological, neurotrophic, neuroendocrine, epigenetic, and neurotranscriptomic features of ADHD, autism, and schizophrenia.
ISBN: 9798645451677Subjects--Topical Terms:
588700
Neurosciences.
Subjects--Index Terms:
Behavior
Developmental Nicotine Exposure Induces Intergenerational Transmission of an Ensemble of Neurodevelopmental Disorder-Like Behavioral, Neuropharmacological, Neurotrophic, Neuroendocrine, Epigenetic, and Neurotranscriptomic Phenotypes in Adolescent Mice.
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Smoking during pregnancy confers liability to neurodevelopmental disorders such as ADHD, autism, and schizophrenia in children and potentially grandchildren as well. Modeling the intergenerationally transmissible phenotypic consequences of smoking during pregnancy, the experiments embodying this thesis examined the behavioral, neuropharmacological, neurobiological, epigenetic, and neurotranscriptomic impacts of developmental nicotine exposure in the adolescent offspring and grandoffspring of nicotine-exposed female mice. Results demonstrate that developmental nicotine exposure elicits multigenerational hyperactivity and risk-taking behaviors, aberrant circadian rhythmicity of activity, enhanced nicotine intake, therapeutic-like behavioral responsivity to methylphenidate and nicotine, corticostriatothalamic nicotinic acetylcholine receptor dysfunction, corticostriatal dopamine transporter dysfunction, impaired corticostriatal proBDNF proteolysis which correlates with furin deficits, corticostriatal glucocorticoid receptor hypoactivity, hypocorticosteronemia, corticostriatal DNA methylome and DNA methyltransferase 3A deficits, downregulation of methyl-CpG-binding protein 2 and histone deacetylase 2 in the frontal cortices and hippocampi, and an array of transcriptomic anomalies in dopamine receptor D1-expressing striatal medium spiny neurons. This phenotypic ensemble recapitulates behavioral, neuropharmacological, neurotrophic, neuroendocrine, epigenetic, and neurotranscriptomic features of ADHD, autism, and schizophrenia.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=27833587
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