ArticleExperimental neurobiology2011
Interactions of Dopamine D1 and N-methyl-D-Aspartate Receptors are Required for Acute Cocaine-Evoked Nitric Oxide Efflux in the Dorsal Striatum.
Article in Experimental neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- D2 receptor activation modulates NMDA receptor antagonist-enhanced high-frequency oscillations in the olfactory bulb of freely moving rats.Psychopharmacology · 2025Article
- Glutamate Transport: A New Bench to Bedside Mechanism for Treating Drug Abuse.The international journal of neuropsychopharmacology · 2017Review
- Chronic cocaine induces HIF-VEGF pathway activation along with angiogenesis in the brain.PloS one · 2017Article
- AMPA receptor upregulation in the nucleus accumbens shell of cocaine-sensitized rats depends upon S-nitrosylation of stargazin.Neuropharmacology · 2014Article
- Cocaine potentiates MDMA-induced oxidative stress but not dopaminergic neurotoxicity in mice: implications for the pathogenesis of free radical-induced neurodegenerative disorders.Psychopharmacology · 2013Article
- Extrasynaptic targeting of NMDA receptors following D1 dopamine receptor activation and cocaine self-administration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Stimulating the addictive brain.Frontiers in human neuroscience · 2012Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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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.
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