Blockage of dopamine D2 receptor in orbitofrontal cortex fails to abolish the performance improving effects of atomoxetine on the spontaneusly hypertensive rat in an attentional set-shifting task

• Main Authors: Jian-Yuan Huang, 黃建源
• Other Authors: Jay-Shake Li
• Format: Others
• Language: zh-TW
• Published: 2013
• Online Access: http://ndltd.ncl.edu.tw/handle/28686950979553036922

碩士 === 國立中正大學 === 心理學研究所 === 101 === Attention-deficit hyperactivity disorder (ADHD) is a clinically heterogeneous disorder. The symptoms include inattention, hyperactivity and impulsivity. Atomoxetine (ATX) is a selective norepinephrine reuptake inhibitor which served as a non-psychostimulant drug for the treatment for ADHD. Previous studies found that ATX increases not only norepinephrine levels but also dopamine levels in prefrontal cortex. The effect of ATX on the dopamine system is similar to methylphenidate, the first-line treatment for ADHD. However, the neural mechanism of ATX treatment of ADHD is still unclear. In experiment 1, we examined the effect of systemic ATX on juvenile SHR and Wistar control in attentional set-shifting task. During reversal learning phase, rats received reinforcements only if they successfully inhibited impulsive responses and learned reversed rules. In experiment 2, we further investigated the effect of central ATX (0.1 μg/0.5 μl/side) in the orbitofrontal cortex (OFC) on juvenile SHR. In order to examine whether the behavior improvement of ATX is indirectly through the dopamine D2 receptors, we applied intra-OFC infusion of haloperidol (0.5 μg/0.4 μl/side) in experiment 3. The results showed that ATX injection through intraperitoneal as well as intra-OFC can remove the reversal learning deficits of SHR. Central infusion of haloperidol in OFC failed to abolish the beneficial effects of ATX. We suggested that the OFC dopamine system might not be involved in the treatment effects of ATX on ADHD.