Involvement of Hippocampal D1-Like Dopamine Receptors in the Inhibitory Effect of Cannabidiol on Acquisition and Expression of Methamphetamine-Induced Conditioned Place Preference

• Published in: Neurochemical research 2021-08, Vol.46 (8), p.2008-2018
• Main Authors: Nouri, Kiana, Anooshe, Mahsa, Karimi-Haghighi, Saeideh, Mousavi, Zahra, Haghparast, Abbas
• Format: Article
• Language: English
• Subjects: Animals; Benzazepines - pharmacology; Biochemistry; Biomedical and Life Sciences; Biomedicine; CA1 Region, Hippocampal - drug effects; CA1 Region, Hippocampal - metabolism; Cannabidiol; Cannabidiol - therapeutic use; Cannabinoids; Cell Biology; Central Nervous System Agents - pharmacology; Circuits; Conditioning; Conditioning, Psychological - drug effects; Dopamine; Dopamine Antagonists - pharmacology; Dopamine D1 receptors; Drug abuse; Hippocampus; Locomotion; Male; Methamphetamine; Methamphetamine - pharmacology; Microinjection; Neurochemistry; Neurology; Neurosciences; Original Paper; Place preference conditioning; Rats; Rats, Wistar; Receptors; Receptors, Dopamine D1 - antagonists & inhibitors; Receptors, Dopamine D1 - metabolism; Reinforcement; Schedules; Side effects
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-021-03350-w

Cannabidiol (CBD) is a non-psychotomimetic compound with strong potential to decrease the psychostimulant’s rewarding effect with unclear receptors. Furthermore, as a part of the reward circuit, the hippocampus plays a crucial role in regulating the reward properties of drugs as determined by conditioned place preference (CPP). In the current research, CPP was used to evaluate the role of intra-CA1 microinjection of D1-like dopamine receptor antagonists in CBD's inhibitory effect on the acquisition and expression phases of methamphetamine (METH). Animals were treated by METH (1 mg/kg; sc) in a five-day schedule to induce CPP. To find out the impact of D1-like dopamine receptor antagonist, SCH23390, in the CA1 on the inhibitory influence of CBD on the acquisition of METH, the rats received intra-CA1 administration of SCH23390 (0.25, 1, and 4 µg/0.5 µl) following ICV treatment of CBD (10 µg/5 µl) over conditioning phase of METH. Furthermore, animals were given SCH23390 in the CA1 ensuing ICV microinjection of CBD (50 µg/5 µl) in the expression phase of METH to rule out the influence of SCH23390 on the suppressive effect of CBD on the expression of METH CPP. Intra-CA1 microinjection of SCH23390 abolished CBD's suppressive impact on both METH-induced CPP phases without any side effect on the locomotion. The current research disclosed that CBD inhibited the rewarding characteristic of METH via D1-like dopamine receptors in the CA1 region of the hippocampus.