Abstract

Beneficial effects of cannabidiol (CBD) have been described for a wide range of psychiatric disorders, including anxiety, psychosis, and depression. The mechanisms responsible for these effects, however, are still poorly understood. Similar to clinical antidepressant or atypical antipsychotic drugs, recent findings clearly indicate that CBD, either acutely or repeatedly administered, induces plastic changes. For example, CBD attenuates the decrease in hippocampal neurogenesis and dendrite spines density induced by chronic stress and prevents microglia activation and the decrease in the number of parvalbumin-positive GABA neurons in a pharmacological model of schizophrenia. More recently, it was found that CBD modulates cell fate regulatory pathways such as autophagy and others critical pathways for neuronal survival in neurodegenerative experimental models, suggesting the potential benefit of CBD treatment for psychiatric/cognitive symptoms associated with neurodegeneration. These changes and their possible association with CBD beneficial effects in psychiatric disorders are reviewed here.

Highlights

  • Plasticity relates to the particular characteristic of a material that undergoes deformation under a load (Lubliner, 2005)

  • Réus et al (2011) reported similar results in three brain regions (PFC, hippocampus, and amygdala) after acute treatment with doses that induced antidepressant-like effects in rats submitted to the Forced Swimming Test (FST)

  • CBD reversed 3-nitropropionic acid-induced reductions in GABA contents and mRNA levels for substance P, neuronal specific enolase and superoxide dismutase 2, effects that were independent of CB1, TRPV1, and A2A receptors (Sagredo et al, 2007)

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Summary

Introduction

Plasticity relates to the particular characteristic of a material that undergoes deformation under a load (Lubliner, 2005). CBD effects were prevented by pharmacological antagonism of CB1 and CB2 receptors, suggesting that the anti-stress effects CBD depend on facilitation of hippocampal neurogenesis through a mechanism that involves increased ECB levels (Campos et al, 2013a). Réus et al (2011) reported similar results in three brain regions (PFC, hippocampus, and amygdala) after acute treatment with doses that induced antidepressant-like effects in rats submitted to the FST.

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