دورية أكاديمية
أعرض في EDS

Developmental nicotine exposure precipitates multigenerational maternal transmission of nicotine preference and ADHD-like behavioral, rhythmometric, neuropharmacological, and epigenetic anomalies in adolescent mice.

التفاصيل البيبلوغرافية
العنوان: Developmental nicotine exposure precipitates multigenerational maternal transmission of nicotine preference and ADHD-like behavioral, rhythmometric, neuropharmacological, and epigenetic anomalies in adolescent mice.
المؤلفون: Buck JM; Institute for Behavioral Genetics, University of Colorado, Boulder, United States; Department of Integrative Physiology, University of Colorado, Boulder, United States. Electronic address: Jordan.Buck@colorado.edu., Sanders KN; Institute for Behavioral Genetics, University of Colorado, Boulder, United States., Wageman CR; Institute for Behavioral Genetics, University of Colorado, Boulder, United States., Knopik VS; Department of Human Development and Family Studies, Purdue University, United States., Stitzel JA; Institute for Behavioral Genetics, University of Colorado, Boulder, United States; Department of Integrative Physiology, University of Colorado, Boulder, United States., O'Neill HC; Institute for Behavioral Genetics, University of Colorado, Boulder, United States.
المصدر: Neuropharmacology [Neuropharmacology] 2019 May 01; Vol. 149, pp. 66-82. Date of Electronic Publication: 2019 Feb 08.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Pergamon Press Country of Publication: England NLM ID: 0236217 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7064 (Electronic) Linking ISSN: 00283908 NLM ISO Abbreviation: Neuropharmacology Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford : Pergamon Press
Original Publication: Oxford, New York, Pergamon.
مواضيع طبية MeSH: Behavior, Animal/*drug effects , Motor Activity/*drug effects , Nicotine/*pharmacology , Prenatal Exposure Delayed Effects/*physiopathology, Adolescent ; Animals ; Attention Deficit Disorder with Hyperactivity ; Corpus Striatum/drug effects ; Disease Models, Animal ; Dopamine/metabolism ; Dopamine Plasma Membrane Transport Proteins/metabolism ; Female ; Frontal Lobe/drug effects ; Humans ; Hyperkinesis ; Methylphenidate/pharmacology ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Receptors, Nicotinic/metabolism ; Self Administration
مستخلص: Maternal smoking during pregnancy, a form of developmental nicotine exposure (DNE), is associated with increased nicotine use and neurodevelopmental disorders such as ADHD in children. Here, we characterize the behavioral, rhythmometric, neuropharmacological, and epigenetic consequences of DNE in the F1 (first) and F2 (second) generation adolescent offspring of mice exposed to nicotine prior to and throughout breeding. We assessed the effects of passive oral methylphenidate (MPH) administration and voluntary nicotine consumption on home cage activity rhythms and activity and risk-taking behaviors in the open field. Results imply a multigenerational predisposition to nicotine consumption in DNE mice and demonstrate ADHD-like diurnal and nocturnal hyperactivity and anomalies in the rhythmicity of home cage activity that are reversibly rescued by MPH and modulated by voluntary nicotine consumption. DNE mice are hyperactive in the open field and display increased risk-taking behaviors that are normalized by MPH. Pharmacological characterization of nicotinic and dopaminergic systems in striatum and frontal cortex reveals altered expression and dysfunction of nicotinic acetylcholine receptors (nAChRs), hypersensitivity to nicotine-induced nAChR-mediated dopamine release, and impaired dopamine transporter (DAT) function in DNE mice. Global DNA methylation assays indicate DNA methylome deficits in striatum and frontal cortex of DNE mice. Collectively, our data demonstrate that DNE enhances nicotine preference, elicits hyperactivity and risk-taking behaviors, perturbs the rhythmicity of activity, alters nAChR expression and function, impairs DAT function, and causes DNA hypomethylation in striatum and frontal cortex of both first and second-generation adolescent offspring. These findings recapitulate multiple domains of ADHD symptomatology.
(Copyright © 2019 Elsevier Ltd. All rights reserved.)
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معلومات مُعتمدة: P30 DA015663 United States DA NIDA NIH HHS; R01 DA003194 United States DA NIDA NIH HHS; R21 DA040228 United States DA NIDA NIH HHS; T32 DA017637 United States DA NIDA NIH HHS
فهرسة مساهمة: Keywords: ADHD; Acetylcholine; Development; Dopamine; Methylation; Nicotine
المشرفين على المادة: 0 (Dopamine Plasma Membrane Transport Proteins)
0 (Receptors, Nicotinic)
207ZZ9QZ49 (Methylphenidate)
6M3C89ZY6R (Nicotine)
VTD58H1Z2X (Dopamine)
تواريخ الأحداث: Date Created: 20190212 Date Completed: 20200127 Latest Revision: 20210109
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC7096676
DOI: 10.1016/j.neuropharm.2019.02.006
PMID: 30742847
قاعدة البيانات: MEDLINE
الوصف
تدمد:1873-7064
DOI:10.1016/j.neuropharm.2019.02.006