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Review examines whether cannabis effects on hippocampus and dopamine pathways explain psychosis risk

ReviewModerate evidence
The takeaway

Cannabis clearly affects hippocampal function and structure, but the evidence that it increases striatal dopamine function, a key mechanism proposed for psychosis, is less robust than commonly assumed.

Psychosis researchers, neuroscientists studying cannabis and dopamine

Hippocampal effects: clear evidence. Striatal dopamine effects: less robust evidence.

What the researchers found

Using the MAM rodent model as a framework, the review found clear evidence that cannabis/cannabinoids affect hippocampal and medial temporal lobe function and structure. However, evidence that cannabis increases striatal dopamine function was less robust. Limited evidence existed for cannabis effects on cortical and striatal glutamate levels.

Why it matters

The dopamine hypothesis is central to understanding psychosis. If cannabis-related psychosis operates through hippocampal dysfunction rather than direct dopamine effects, it could change therapeutic approaches.

The numbers in context

No specific pooled statistics; the review synthesizes evidence across imaging and preclinical studies and finds the hippocampal evidence stronger than the striatal dopamine evidence.

How the study worked

Review using the methylazoxymethanol acetate (MAM) rodent model of psychosis as a framework to examine cannabis effects on hippocampal-striatal-dopamine pathways. Examines neuroimaging and preclinical evidence.

What this study cannot tell us

Relies on animal model as framework; limited human neuroimaging studies directly testing the proposed pathway; the MAM model may not perfectly recapitulate cannabis-related psychosis.

How to read the evidence

Focused review using a preclinical framework to organize human and animal evidence.

When this study was published

Published in 2020.

The bigger picture

The distinction between clear hippocampal effects and weaker dopamine evidence suggests the cannabis-psychosis pathway may be more nuanced than a simple "cannabis increases dopamine" narrative.

Questions still open

  • Could hippocampal dysfunction be the primary mediator of cannabis-related psychosis risk? Would multimodal neuroimaging studies better capture the proposed pathway?

Common questions

Does cannabis increase dopamine and cause psychosis?
The review found that while cannabis clearly affects the hippocampus, the evidence that it directly increases striatal dopamine function is less robust than often assumed. The pathway from cannabis to psychosis may run through hippocampal dysfunction rather than direct dopamine elevation.
What is the MAM model?
The methylazoxymethanol acetate (MAM) model is a well-established rodent model of psychosis that produces hippocampal dysfunction leading to increased dopamine activity. The review uses this model as a framework to ask whether cannabis might produce similar effects.

Read the original research

Do the effects of cannabis on the hippocampus and striatum increase risk for psychosis?

Neuroscience and biobehavioral reviews, 112, 324-335

Citation

Daniju, Y; Bossong, M G; Brandt, K; Allen, P. (2020). Do the effects of cannabis on the hippocampus and striatum increase risk for psychosis?. Neuroscience and biobehavioral reviews, 112, 324-335. https://doi.org/10.1016/j.neubiorev.2020.02.010

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