@article{ref1,
title="On the Role of Cannabinoid CB1- and μ-Opioid Receptors in Motor Impulsivity",
journal="Frontiers in pharmacology",
year="2012",
author="Wiskerke, Joost and van Mourik, Yvar and Schetters, Dustin and Schoffelmeer, Anton N. M. and Pattij, Tommy",
volume="3",
number="",
pages="108-108",
abstract="Previous studies using a rat 5-choice serial reaction time task have established a critical role for dopamine D2 receptors in regulating increments in motor impulsivity induced by acute administration of the psychostimulant drugs amphetamine and nicotine. Here we investigated whether cannabinoid CB1 and/or μ-opioid receptors are involved in nicotine-induced impulsivity, given recent findings indicating that both receptor systems mediate amphetamine-induced motor impulsivity. Results showed that the cannabinoid CB1 receptor antagonist SR141716A, but not the opioid receptor antagonist naloxone, reduced nicotine-induced premature responding, indicating that nicotine-induced motor impulsivity is cannabinoid, but not opioid receptor-dependent. In contrast, SR141716A did not affect impulsivity following a challenge with the dopamine transporter inhibitor GBR 12909, a form of drug-induced impulsivity that was previously found to be dependent on μ-opioid receptor activation. Together, these data are consistent with the idea that the endogenous cannabinoid, dopamine, and opioid systems each play important, but distinct roles in regulating (drug-induced) motor impulsivity. The rather complex interplay between these neurotransmitter systems modulating impulsivity will be discussed in terms of the differential involvement of mesocortical and mesolimbic neurocircuitry.<p /> <p>Language: en</p>",
language="en",
issn="1663-9812",
doi="10.3389/fphar.2012.00108",
url="http://dx.doi.org/10.3389/fphar.2012.00108"
}