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Cannabis points to the synaptic pathology of mental disorders: how aberrant synaptic components disrupt the highest psychological functions .

Paul D. Morrison, Robin Murray

Dialogues in Clinical Neuroscience September 2020 DOI: 10.31887/dcns.2020.22.3/pmorrison (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Cannabis Ketamine
Keywords Bipolar Cognition Connectome Dendritic spine Plasticity Psychosis Schizophrenia ∆9-tetrahydrocannabinol
Key findings Argues that delta-9-tetrahydrocannabinol disrupts neuronal dynamics and synaptic plasticity by acting on CB1 receptors at glutamate and GABA neuron terminals, causing cognitive deficits and impairment of higher psychological functions. The authors contend that ketamine and methamphetamine act in the same synaptic spine microdomain, and that psychiatric genetics findings often involve dendritic spine components tied to information processing and plasticity.

Abstract

Cannabis can elicit an acute psychotic reaction, and its long-term use is a risk factor for schizophrenia. The main active psychoactive ingredient ∆9-tetrahydrocannabinol (Δ9-THC) activates cannabinoid 1 (CB1) receptors, which are localized to the terminals of glutamate and GABA neurons in the brain. The endogenous cannabinoids are involved in information processing and plasticity at synapses in the hippocampus, basal ganglia, and cerebral cortex. Exogenously applied CB1 receptor agonists disrupt neuronal dynamics and synaptic plasticity, resulting in cognitive deficits and impairment of the highest psychological functions. Various other pro-psychotic drugs, such as ketamine and methamphetamine, exert their effects in the same microdomain of synaptic spines as Δ9-THC. Additionally, many of the most robust findings in psychiatric genetics include components that localize to dendritic spines and have important roles in information processing and plasticity. .

Comparable studies

Other narrative reviews on cannabis, most cited first.

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