ArticleNeurochemical research2021
The Adenosine A2A Receptor Activation in Nucleus Accumbens Suppress Cue-Induced Reinstatement of Propofol Self-administration in Rats.
Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Microglial Activation Is Associated with Hippocampal Synaptic Degeneration and Cognitive Deficits Following Repeated Propofol Exposure.International journal of molecular sciences · 2026Article
- Adenosine APsychopharmacology · 2026Article
- Dopamine D2 Receptors, D1/D2 Receptor Heteromers and CaMKII Signaling in the Neurobiology of Drug Addiction.Molecular neurobiology · 2026Review
- The Role of Toll-like Receptor 3 Signaling in Cognitive Impairment Induced by Propofol Addiction.Molecular neurobiology · 2025Article
- A comprehensive analysis of propofol abuse, addiction and neuropharmacological aspects: an updated review.Korean journal of anesthesiology · 2025Review
- Effects of intravenous propofol combined with opioids on euphoria in patients undergoing painless gastrointestinal endoscopy: protocol for a randomized double-blind placebo-controlled trial.Frontiers in pharmacology · 2025Article
- Non-Opioid Anesthetics Addiction: A Review of Current Situation and Mechanism.Brain sciences · 2023Review
- The Antagonism of Corticotropin-Releasing Factor Receptor-1 in Brain Suppress Stress-Induced Propofol Self-Administration in Rats.Frontiers in behavioral neuroscience · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Propofol has shown strong addictive properties in rats and humans. Adenosine A2A receptors (A2AR) in the nucleus accumbens (NAc) modulate dopamine signal and addictive behaviors such as cocaine- and amphetamine-induced self-administration. However, whether A2AR can modulate propofol addiction remains unknown. AAV-shA2AR was intra-NAc injected 3 weeks before the propofol self-administration training to test the impacts of NAc A2AR on establishing the self-administration model with fixed ratio 1 (FR1) schedule. Thereafter, the rats were withdrawal from propofol for 14 days and tested cue-induced reinstatement of propofol seeking behavior on day 15. The propofol withdrawal rats received one of the doses of CGS21680 (A2AR agonist, 2.5-10.0 ng/site), MSX-3 (A2AR antagonist, 5.0-20.0 μg/site) or eticlopride (D2 receptor (D2R) antagonist, 0.75-3.0 μg/site) or vehicle via intra-NAc injection before relapse behavior test. The numbers of active and inactive nose-poke response were recorded. Focal knockdown A2AR by shA2AR did not affect the acquisition of propofol self-administration behavior, but enhance cue-induced reinstatement of propofol self-administration compared with the AAV-shCTRLgroup. Pharmacological activation of the A2AR by CGS21680 (≥ 5.0 ng/site) attenuated cue-induced reinstatement of propofol self-administration behavior. Similarly, pharmacological blockade of D2R by eticlopride (0.75-3.0 μg/site) attenuated propofol seeking behavior. These effects were reversed by the administration of MSX-3 (5.0-20.0 μg/site). The A2AR- and D2R-mediated effects on propofol relapse were not confounded by the learning process, and motor activity as the sucrose self-administration and locomotor activity were not affected by all the treatments. This study provides genetic and pharmacological evidence that NAc A2AR activation suppresses cue-induced propofol relapse in rats, possibly by interacting with D2R.
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