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Prenatal nicotine exposure mouse model showing hyperactivity, reduced cingulate cortex volume, reduced dopamine turnover, and responsiveness to oral methylphenidate treatment.

Title: Prenatal nicotine exposure mouse model showing hyperactivity, reduced cingulate cortex volume, reduced dopamine turnover, and responsiveness to oral methylphenidate treatment.
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Name(s): Zhu, Jinmin, author
Zhang, Xuan, author
Xu, Yuehang, author
Spencer, Thomas J, author
Biederman, Joseph, author
Bhide, Pradeep G, author
Type of Resource: text
Genre: Journal Article
Text
Date Issued: 2012-07-04
Physical Form: computer
online resource
Extent: 1 online resource
Language(s): English
Abstract/Description: Cigarette smoking, nicotine replacement therapy, and smokeless tobacco use during pregnancy are associated with cognitive disabilities later in life in children exposed prenatally to nicotine. The disabilities include attention deficit hyperactivity disorder (ADHD) and conduct disorder. However, the structural and neurochemical bases of these cognitive deficits remain unclear. Using a mouse model we show that prenatal nicotine exposure produces hyperactivity, selective decreases in cingulate cortical volume, and radial thickness, as well as decreased dopamine turnover in the frontal cortex. The hyperactivity occurs in both male and female offspring and peaks during the "active" or dark phase of the light/dark cycle. These features of the mouse model closely parallel the human ADHD phenotype, whether or not the ADHD is associated with prenatal nicotine exposure. A single oral, but not intraperitoneal, administration of a therapeutic equivalent dose (0.75 mg/kg) of methylphenidate decreases the hyperactivity and increases the dopamine turnover in the frontal cortex of the prenatally nicotine exposed mice, once again paralleling the therapeutic effects of this compound in ADHD subjects. Collectively, our data suggest that the prenatal nicotine exposure mouse model has striking parallels to the ADHD phenotype not only in behavioral, neuroanatomical, and neurochemical features, but also with respect to responsiveness of the behavioral phenotype to methylphenidate treatment. The behavioral, neurochemical, and anatomical biomarkers in the mouse model could be valuable for evaluating new therapies for ADHD and mechanistic investigations into its etiology.
Identifier: FSU_pmch_22764249 (IID), 10.1523/JNEUROSCI.1041-12.2012 (DOI), PMC3417040 (PMCID), 22764249 (RID), 22764249 (EID), 32/27/9410 (PII)
Grant Number: P30 NS045776, R01 DA020796, P30NS045776, R01DA020796, R21DA027358, R21 DA027358
Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3417040.
Subject(s): Animals
Attention Deficit Disorder with Hyperactivity/chemically induced
Attention Deficit Disorder with Hyperactivity/drug therapy
Attention Deficit Disorder with Hyperactivity/physiopathology
Disease Models, Animal
Dopamine/metabolism
Female
Gyrus Cinguli/drug effects
Gyrus Cinguli/pathology
Gyrus Cinguli/physiopathology
Male
Methylphenidate/pharmacology
Mice
Mice, Inbred C57BL
Models, Neurological
Nicotine/toxicity
Pregnancy
Prenatal Exposure Delayed Effects/chemically induced
Prenatal Exposure Delayed Effects/pathology
Prenatal Exposure Delayed Effects/physiopathology
Smoking/adverse effects
Persistent Link to This Record: http://purl.flvc.org/fsu/fd/FSU_pmch_22764249
Owner Institution: FSU
Is Part Of: The Journal of neuroscience : the official journal of the Society for Neuroscience.
1529-2401
Issue: iss. 27, vol. 32

Choose the citation style.
Zhu, J., Zhang, X., Xu, Y., Spencer, T. J., Biederman, J., & Bhide, P. G. (2012). Prenatal nicotine exposure mouse model showing hyperactivity, reduced cingulate cortex volume, reduced dopamine turnover, and responsiveness to oral methylphenidate treatment. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience. Retrieved from http://purl.flvc.org/fsu/fd/FSU_pmch_22764249