Imaging the Effects of Methylphenidate on Brain Dopamine: New Model on Its Therapeutic Actions for Attention-Deficit/Hyperactivity Disorder

Volkow, Nora D.; Wang, Gene‐Jack; Fowler, Joanna S.; Ding, Yu‐Shin

doi:10.1016/j.biopsych.2004.11.006

Cited by 316 publications

(250 citation statements)

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“…In line with the previous literature, nicotine reduced activation without worsening performance, a pattern which may be interpreted as more efficient processing (Newhouse et al, 2011;Wylie et al, 2012), whereas the increase in activation in absence of performance improvement under methylphenidate could be interpreted in the context of task saliency (Volkow et al, 2005).…”

Section: Discussionsupporting

confidence: 89%

“…Activation of the FEFs, as observed more strongly in our methylphenidate group compared to the nicotine group, has been associated with spatial attention (Corbetta et al, 1998) and the voluntary control of eye movements (Pierrot-Deseilligny et al, 2004). An enhancement of such task-related activation would be in line with previously demonstrated effects of methylphenidate on task saliency (Farr et al, 2014;Linssen et al, 2014;Volkow et al, 2005). Increased activation of parietal and frontal eye fields has also been observed in tasks requiring suppression of visual background distractors (Kimmig et al, 2008;Ohlendorf et al, 2010).…”

Section: Accepted M Manuscriptsupporting

confidence: 87%

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Neural effects of methylphenidate and nicotine during smooth pursuit eye movements

et al. 2016

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Citation for published version (APA):Kasparbauer, A-M., Meyhöfer, I., Steffens, M., Weber, B., Aydin, M., Kumari, V., ... Ettinger, U. (2016). Neural effects of methylphenidate and nicotine during smooth pursuit eye movements. NeuroImage. DOI: 10.1016DOI: 10. /j.neuroimage.2016 Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rightsCopyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights.•Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research.•You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policy If you believe that this document breaches copyright please contact librarypure@kcl.ac.uk providing details, and we will remove access to the work immediately and investigate your claim. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPT AbstractIntroduction: Nicotine and methylphenidate are putative cognitive enhancers in healthy and patient populations. Although they stimulate different neurotransmitter systems, they have been shown to enhance performance on overlapping measures of attention. So far, there has been no direct comparison of the effects of these two stimulants on behavioural performance or brain function in healthy humans. Here, we directly compare the two compounds using a wellestablished oculomotor biomarker in order to explore common and distinct behavioural and neural effects. Methods: Eighty-two healthy male non-smokers performed a smooth pursuit eye movement task while lying in an fMRI scanner. In a between-subjects, double-blind design, subjects either received placebo (placebo patch and capsule), nicotine (7mg nicotine patch and placebo capsule), or methylphenidate (placebo patch and 40mg methylphenidate capsule).Results: There wer...

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Section: Discussionsupporting

confidence: 89%

Section: Accepted M Manuscriptsupporting

confidence: 87%

Neural effects of methylphenidate and nicotine during smooth pursuit eye movements

et al. 2016

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“…From a clinical perspective, it is interesting to note that methylphenidate (Ritalin s ) is the most commonly prescribed pharmacotherapy for attention-deficit/hyperactivity disorder (ADHD), a behavioral disorder characterized by excessive levels of activity, impulsivity, and inattention (Arnsten, 2006;Solanto et al, 2001;Volkow et al, 2005). Methylphenidate is an effective treatment for the behavioral and cognitive deficits associated with ADHD when administered orally at therapeutic doses (Greenhill, 2001;Volkow and Swanson, 2003;Biederman et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Wooters

Neugebauer

Rush

et al. 2007

Neuropsychopharmacol

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Stimulant drugs, including D-amphetamine, cocaine, and methylphenidate, increase cigarette smoking in controlled human laboratory experiments. Although the mechanism(s) underlying this effect are unknown, it is possible that stimulants may enhance directly the abuse-related effects of nicotine. In the present study, we characterized the behavioral pharmacological interactions between methylphenidate and nicotine in the intravenous self-administration, drug discrimination, and locomotor cross-sensitization procedures. Adult male Sprague-Dawley rats were trained to respond for intravenous nicotine (0.01 or 0.03 mg/kg/infusion) or sucrose, and the acute effects of methylphenidate (1.25-10 mg/kg) were determined; in addition, separate groups of rats were treated with methylphenidate (2.5 mg/kg) or saline before 12 consecutive nicotine (0.03 mg/kg/infusion) self-administration sessions. Next, the discriminative stimulus effects of nicotine (0.03-0.3 mg/kg) and methylphenidate (1.25-10 mg/kg), alone and in combination with a low nicotine dose (0.056 mg/kg), were tested in nicotine-trained rats. Finally, the locomotor effect of repeated methylphenidate (2.5 mg/kg) was tested in rats previously treated with nicotine (0.2-0.8 mg/kg). Results indicated that acute methylphenidate increased the rate of nicotine self-administration at doses that reduced sucrose-maintained responding; furthermore, tolerance to this effect was not apparent following repeated methylphenidate. Methylphenidate, while not substituting for nicotine alone, dose-dependently enhanced the discriminative stimulus effect of a low nicotine dose. In addition, repeated nicotine exposure promoted the development of locomotor sensitization to methylphenidate. Taken together with recent clinical findings, these results suggest that methylphenidate may enhance the abuse-related behavioral effects of nicotine, perhaps increasing vulnerability to tobacco dependence.

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“…Ainsi, le méthylphénidate (Ritaline ® , Concerta ® ) augmente la concentration de dopamine dans la fente synaptique par l'intermédiaire du blocage du transporteur de la dopamine (DAT). Les données d'imagerie fonctionnelle montrent que cette augmentation de dopamine extracellulaire est plus grande après exposition à un stimulus environnemental ayant une valeur de renforcement (test mathématique) qu'après un stimulus neutre [12]. L'hypothèse proposée par les auteurs serait que l'augmentation extracellulaire de dopamine au niveau des neurones striataux diminuerait leur activité de base aléatoire et permettrait aux afférences cortico-striatales liées aux stimulus pertinents d'être plus efficaces (Figure 1).…”

Section: Les Mécanismes Neurobiologiquesunclassified

Neurobiologie du trouble déficit de l’attention/ hyperactivité

et al. 2010

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Imaging the Effects of Methylphenidate on Brain Dopamine: New Model on Its Therapeutic Actions for Attention-Deficit/Hyperactivity Disorder

Cited by 316 publications

References 47 publications

Neural effects of methylphenidate and nicotine during smooth pursuit eye movements

Neural effects of methylphenidate and nicotine during smooth pursuit eye movements

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Neurobiologie du trouble déficit de l’attention/ hyperactivité

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