A non-psychoactive cannabis extract sped up extinction of cocaine preference and blocked cocaine-primed relapse in mice, working through serotonin receptors rather than cannabinoid receptors.
Addiction researchers, scientists studying cannabinoid therapeutics, substance use treatment developers
Cannabis extract blocked cocaine relapse; pure CBD did not
What the researchers found
A non-psychoactive cannabis extract (NPCE) significantly reduced the extinction latency of smoked cocaine-induced place preference, while pure CBD did not. NPCE also selectively blocked relapse triggered by a priming dose of cocaine but not stress-induced relapse. The serotonin 5-HT1A receptor was involved in this effect, while the CB2 receptor was not.
Why it matters
Smoked cocaine (crack) is particularly addictive and difficult to treat. Finding that a non-psychoactive cannabis extract reduces relapse markers in a relevant animal model opens a potential new treatment avenue.
The numbers in context
NPCE reduced extinction latency of AEME-COC preference (CBD did not). NPCE blocked priming-dose reinstatement but not stress-induced reinstatement. 5-HT1A receptor antagonist attenuated NPCE effects. CB2 receptor inverse agonist had no significant impact.
How the study worked
Mouse conditioned place preference model using AEME-COC (a model for smoked cocaine). Three experiments tested: (1) cocaine vs AEME-COC conditioning, (2) CBD vs NPCE on extinction, (3) receptor antagonists on NPCE-mediated inhibition of reinstatement. Behavioral pharmacology approaches identified receptor mechanisms.
What this study cannot tell us
Animal model of cocaine preference does not fully capture human addiction. NPCE composition may vary between preparations. IP administration does not mimic human use. Single study requiring replication.
How to read the evidence
Preliminary: animal study using a conditioned place preference model with a single non-psychoactive cannabis extract preparation
When this study was published
Published in 2025
The bigger picture
The fact that a whole cannabis extract worked where isolated CBD did not suggests that other non-psychoactive compounds in the plant may contribute to anti-addiction effects. The serotonin mechanism provides a pathway for future drug development.
Questions still open
- Which specific non-psychoactive compounds in the extract are responsible? Would oral NPCE administration produce the same effects? Could this approach translate to human crack cocaine treatment?
Common questions
Why did the cannabis extract work but pure CBD did not?
Could cannabis-based treatments help with cocaine addiction?
Read the original research
Non-psychoactive cannabis extract promotes extinction and reduces reinstatement by priming dose in smoked cocaine-induced conditioned place preference.
Physiology & behavior, 301, 115048
Citation
Barreto, Fabián Leonardo; Lozano, María Constanza; Martínez-Ramírez, Jorge A. (2025). Non-psychoactive cannabis extract promotes extinction and reduces reinstatement by priming dose in smoked cocaine-induced conditioned place preference.. Physiology & behavior, 301, 115048. https://doi.org/10.1016/j.physbeh.2025.115048
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