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Neural mechanisms underlying psilocybin’s therapeutic potential – the need for preclinical in vivo electrophysiology

Summary

Psilocybin, the active compound in magic mushrooms, shows promise for treating depression and other mental health conditions. This review examines how psilocybin works in the brain, particularly by affecting brain regions involved in self-reflection and emotion regulation. The authors argue that new brain recording techniques are needed to fully understand how psilocybin produces its beneficial effects, which could help improve treatments for people with severe depression.

Background

Psilocybin is a naturally occurring psychedelic compound with profound effects on perception, emotion, and cognition that shows promise for treating brain disorders. However, the neural mechanisms mediating its therapeutic effects require deeper investigation to understand how psychedelics produce their profound and long-lasting effects.

Objective

This review aims to summarize current understanding of psilocybin’s neurophysiology by describing how it affects brain regions associated with the default-mode network (DMN), particularly the prefrontal cortex and hippocampus, and to argue for the need for preclinical in vivo electrophysiology studies.

Results

Evidence shows psilocybin decreases activity in prefrontal and posterior cingulate cortices while potentially increasing glutamatergic signaling and GABA release. Studies indicate psychedelics increase gamma oscillatory power and decrease low-frequency delta oscillations, though region-specific and compound-specific differences exist.

Conclusion

In vivo electrophysiology is ideally suited to provide holistic neural network analysis of psilocybin’s mode of action. Understanding psilocybin-induced changes in neural oscillatory activity is crucial for determining the mechanisms underlying its therapeutic potential for treatment-resistant depression and other difficult-to-treat conditions.
  • Published in:Journal of Psychopharmacology,
  • Study Type:Review,
  • Source: PMID: 35638159, DOI: 10.1177/02698811221092508
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