Open AccessCannabis points to the synaptic pathology of mental disorders: how aberrant synaptic components disrupt the highest psychological functions
Author(s) -
Paul Morrison,
Robin M. Murray
Publication year - 2020
Publication title -
dialogues in clinical neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.11
H-Index - 87
eISSN - 1958-5969
pISSN - 1294-8322
DOI - 10.31887/dcns.2020.22.3/pmorrison
Subject(s) - synaptic plasticity , neuroscience , cannabinoid receptor , dendritic spine , glutamate receptor , hippocampus , cannabinoid , schizophrenia (object oriented programming) , neuroplasticity , psychosis , psychology , synaptic fatigue , nmda receptor , long term potentiation , synaptic scaling , metaplasticity , biology , hippocampal formation , psychiatry , receptor , agonist , biochemistry
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 (Δ 9 -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 CB 1 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 Δ 9 -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.
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