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dc.contributor.advisorSchachtman, Todd R.eng
dc.contributor.advisorMiller, Dennis K. (Dennis Keith)eng
dc.contributor.authorDopheide, Marsha M.eng
dc.date.issued2007eng
dc.date.submitted2007 Summereng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionTitle from title screen of research.pdf file (viewed on December 20, 2007)eng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionThesis (Ph. D.) University of Missouri-Columbia 2007.eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Modafinil is a novel wake-promoting compound currently marketed as a stimulant that lacks the side effects and addictive potential of typical psychostimulants. Despite these claims, the true mechanism(s) of action for modafinil has yet to be determined. Since modafinil and nicotine share many behavioral, cognitive, and reinforcing effects, this study examined the extent that their pharmacodynamics would also be similar. [³H]Dopamine (DA) overflow (i.e., a measure of DA release) from rat striatal slices preloaded with [³H]DA was used to provide an assessment of whether modafinil, like nicotine, is mediated by nicotinic acetylcholine receptors (nAChRs) or, like amphetamine and cocaine, is mediated by the dopamine transporter (DAT). By observing modafinilevoked [³H]DA overflow in the presence and absence of a variety of nAChR or DAT agonists and antagonists/inhibitors, these experiments examined the degree to which modafinil is mediated by nAChRs or the DAT. Results indicated that modafinil (100-300 µM) evoked [³H]DA overflow in a concentration-dependent manner, but was less potent and efficacious than nicotine, amphetamine, and cocaine. Modafinil-evoked overflow was not altered by the nAChR antagonist mecamylamine and modafinil did not alter nicotine-evoked [³H]DA overflow, making it unlikely that nAChRs are important for modafinil's mechanism of action. The DAT inhibitor nomifensine (10 µM) attenuated (~50%) modafinil-evoked [³H]DA overflow, and concentrations that did not have intrinsic activity attenuated amphetamine (1 and 3 µM) - evoked [³H]DA overflow. Thus, modafinil is pharmacologically similar to, but less potent than, amphetamine and cocaine; however, the behavioral effects are likely mediated through, but not exclusively influenced by, interactions with the DAT.eng
dc.identifier.merlinb61540444eng
dc.identifier.oclc184952916eng
dc.identifier.urihttps://hdl.handle.net/10355/5952
dc.identifier.urihttps://doi.org/10.32469/10355/5952eng
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcommunityUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.rightsAccess is limited to the campus of the University of Missouri--Columbia.eng
dc.subjectpsychosimulants.eng
dc.subjectpsychosimulantseng
dc.subject.lcshDopamineeng
dc.subject.lcshDrugs -- Physiological effecteng
dc.subject.lcshRats -- Effects of drugs oneng
dc.titleThe effect of modafinil on psychostimulant-evoked [³H]dopamine release from rat striatal sliceseng
dc.typeThesiseng
thesis.degree.disciplinePsychological sciences (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


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