Interactions of Dopamine D1 and N-methyl-D-Aspartate Receptors are Required for Acute Cocaine-Evoked Nitric Oxide Efflux in the Dorsal Striatum.
- Author:
Dong Kun LEE
1
;
Sung Min AHN
;
Yoon Bo SHIM
;
Wei Choon Alvin KOH
;
Insop SHIM
;
Eun Sang CHOE
Author Information
- Publication Type:Original Article
- Keywords: addiction; caudate-putamen; dopamine; glutamate; psychostimulant
- MeSH: Benzazepines; Cocaine; Dizocilpine Maleate; Dopamine; Glutamic Acid; N-Methylaspartate; Nitric Oxide; Plastics; Quinpirole; Receptors, Dopamine D1; Receptors, Dopamine D2; Receptors, N-Methyl-D-Aspartate; Up-Regulation
- From:Experimental Neurobiology 2011;20(2):116-122
- CountryRepublic of Korea
- Language:English
- 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.
