Articles

Article

Original Article

Exp Neurobiol 2011; 20(2): 116-122

Published online June 30, 2011

https://doi.org/10.5607/en.2011.20.2.116

© The Korean Society for Brain and Neural Sciences

Interactions of Dopamine D1 and N-methyl-D-Aspartate Receptors Are Required for Acute Cocaine-Evoked Nitric Oxide Efflux in the Dorsal Striatum

Dong Kun Lee1, Sung Min Ahn1, Yoon-Bo Shim2, Wei Choon Alvin Koh2, Insop Shim3 and Eun Sang Choe1*

Departments of 1Biological Sciences, and 2Chemistry, Pusan National University, Busan 609-735, 3Lab of Neuroscience, AMSRC, Kyung Hee University, Seoul 130-701, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 82-51-510-2272, FAX: 82-51-581-2962
e-mail: eschoe@pusan.ac.kr

Abstract

Alterations in nitric oxide (NO) release in response to psychostimulants in the striatum cause a plastic change contributing to the development and expression of addiction. In this study, regulation of NO efflux evoked by acute cocaine in the dorsal striatum was investigated using real-time detection of NO in vivo. We found that acute systemic injection of cocaine (20 mg/kg) increased NO efflux, which was reduced by the intrastriatal infusion of the dopamine D1 receptor antagonist, SCH23390 (7.5 nmol), and the dopamine D2 receptor agonist, quinpirole (5 nmol). Increased levels of NO efflux by acute cocaine were also reduced by the intrastriatal infusion of the N-methyl-D-aspartate (NMDA) receptor antagonists, MK801 (2 nmol) and AP5 (2 nmol). These findings suggest that interactions of dopamine D1 receptors and NMDA receptors after acute exposure to cocaine participate in the upregulation of NO efflux in the dorsal striatum.

Keywords: addiction, caudate-putamen, dopamine, glutamate, psychostimulant