Abstract

Event Abstract Back to Event Dopaminergic modulates task performance and learning-induced plasticity via distinct D1 and D2 receptors Kay Tye1*, Lynne Tye2, Jackson Cone1, Patricia Janak1 and Antonello Bonci1 1 Gallo Center at UCSF, United States 2 MIT, United States Dopamine is thought to contribute to many behavioral actions, including those related to motivation and reward. Methylphenidate (MPH), also known as Ritalin, is currently the most commonly prescribed psychostimulant, but despite prevalent use in children, adolescents and adults, the neural mechanisms by which MPH modifies behavioral performance are unknown for two main reasons. First, MPH is typically administered systemically, thereby altering the function of multiple neural circuits, making it difficult to identify the brain changes that influence behavior. Second, MPH has multiple pharmacological targets, including the dopamine, norepinephrine and serotonin transporters. Previously, we have demonstrated that the lateral amygdala shows a robust, linear relationship between learning performance and synaptic strength. Furthermore, dopamine receptor activation has been shown to enhance amygdala-mediated behaviors. To investigate the acute effects of MPH on behavior as well as learning-induced plasticity, we infused MPH into the amygdala immediately prior to training in a cue-reward task for a natural reward. We found that MPH locally administered in the lateral amygdala enhances learning performance in a similar manner to a selective DAT inhibitor. Additionally, we show that MPH enhances performance both by facilitating the ability to acquire a cue-reward association, via a dopamine D1 receptor-dependent mechanism, as well as by suppressing task-irrelevant behavior, via D2 receptor-dependent mechanisms. Furthermore, we demonstrate that treatment with either MPH or a selective DAT inhibitor elevates levels of DA which gate learning-induced plasticity at cortico-amygdala synapses. This represents a novel mechanism by which MPH enhances learning performance. Conference: 41st European Brain and Behaviour Society Meeting, Rhodes Island, Greece, 13 Sep - 18 Sep, 2009. Presentation Type: Oral Presentation Topic: Symposia lectures Citation: Tye K, Tye L, Cone J, Janak P and Bonci A (2009). Dopaminergic modulates task performance and learning-induced plasticity via distinct D1 and D2 receptors. Conference Abstract: 41st European Brain and Behaviour Society Meeting. doi: 10.3389/conf.neuro.08.2009.09.058 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 05 Jun 2009; Published Online: 05 Jun 2009. * Correspondence: Kay Tye, Gallo Center at UCSF, Emeryville, United States, ktye@gallo.ucsf.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Kay Tye Lynne Tye Jackson Cone Patricia Janak Antonello Bonci Google Kay Tye Lynne Tye Jackson Cone Patricia Janak Antonello Bonci Google Scholar Kay Tye Lynne Tye Jackson Cone Patricia Janak Antonello Bonci PubMed Kay Tye Lynne Tye Jackson Cone Patricia Janak Antonello Bonci Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

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