There is now growing evidence that cannabis use causes a small but reliable increase in the chance of developing psychosis. Traditionally, this was explained by the drug increasing dopamine levels in the brain but a new study shortly to be published in NeuroImage suggests that the active ingredient in cannabis doesn’t effect this important neurotransmitter.
Despite some dissenting voices, disruption to the mesolimbic dopamine pathway is widely thought to be the key problem in the development of delusions, hallucinations and the other psychotic symptoms commonly diagnosed as schizophrenia.
This has led to the assumption that the small increased risk of psychosis reliably associated with cannabis use is due to the drug increasing dopamine levels in a deep brain structure called the striatum.
In itself, this is partly based on another assumption – the virtual mantra of recreational drug research that ‘all drugs of abuse increase dopamine levels in the reward system’ of which the striatum is a part.
This new study, led by neuroscientist Paul Stokes, tested dopamine levels by using a type of PET brain scan where participants are injected with a radioactive tracer that binds to free dopamine receptors. Higher dopamine levels will mean that there are less free dopamine receptors and, therefore, lower tracer levels.
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