Sub-acute effects of psilocybin on EEG correlates of neural plasticity in major depression: Relationship to symptoms.


Journal

Journal of psychopharmacology (Oxford, England)
ISSN: 1461-7285
Titre abrégé: J Psychopharmacol
Pays: United States
ID NLM: 8907828

Informations de publication

Date de publication:
07 2023
Historique:
medline: 14 7 2023
pubmed: 1 7 2023
entrez: 1 7 2023
Statut: ppublish

Résumé

Evidence suggests that serotonergic psychedelics (e.g. psilocybin), have rapid-acting and long-lasting antidepressant effects after a single dose. However, the mechanism underlying these effects remain unclear. One proposed mechanism is that these drugs promote neuroplasticity. However, this has not been conclusively demonstrated in humans. We hypothesized that relative to placebo, psilocybin would: (1) increase electroencephalographic (EEG) correlates of neuroplasticity, (2) reduce depression symptoms, and (3) changes in EEG would correlate with improvements in depression. In this double-blind, placebo-controlled, within-subject study, individuals with major depressive disorder (MDD; EEG theta power doubled in amplitude 2 weeks after a single psychedelic dose of psilocybin but not after placebo. Further, improvements in depression symptoms 2 weeks after psilocybin were correlated with increases in theta power. The increased theta power observed represents evidence of sustained changes in the brain following psilocybin. Given the correlation with enhancement in depressive symptoms, changes in theta may represent an EEG biomarker of the sustained effects of psilocybin, and may shed light on potential mechanisms of psilocybin's antidepressant effect. Taken together, these results complement the emerging notion that psilocybin, and perhaps other psychedelics, can produce long-term alterations in neuroplasticity.

Sections du résumé

BACKGROUND
Evidence suggests that serotonergic psychedelics (e.g. psilocybin), have rapid-acting and long-lasting antidepressant effects after a single dose. However, the mechanism underlying these effects remain unclear. One proposed mechanism is that these drugs promote neuroplasticity. However, this has not been conclusively demonstrated in humans.
AIMS
We hypothesized that relative to placebo, psilocybin would: (1) increase electroencephalographic (EEG) correlates of neuroplasticity, (2) reduce depression symptoms, and (3) changes in EEG would correlate with improvements in depression.
METHODS
In this double-blind, placebo-controlled, within-subject study, individuals with major depressive disorder (MDD;
RESULTS
EEG theta power doubled in amplitude 2 weeks after a single psychedelic dose of psilocybin but not after placebo. Further, improvements in depression symptoms 2 weeks after psilocybin were correlated with increases in theta power.
CONCLUSIONS
The increased theta power observed represents evidence of sustained changes in the brain following psilocybin. Given the correlation with enhancement in depressive symptoms, changes in theta may represent an EEG biomarker of the sustained effects of psilocybin, and may shed light on potential mechanisms of psilocybin's antidepressant effect. Taken together, these results complement the emerging notion that psilocybin, and perhaps other psychedelics, can produce long-term alterations in neuroplasticity.

Identifiants

pubmed: 37392016
doi: 10.1177/02698811231179800
doi:

Substances chimiques

Psilocybin 2RV7212BP0
Hallucinogens 0
Antidepressive Agents 0

Types de publication

Randomized Controlled Trial Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

687-697

Auteurs

Patrick D Skosnik (PD)

Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
VA Connecticut Healthcare System, Newington, USA.

Jordan Sloshower (J)

Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
VA Connecticut Healthcare System, Newington, USA.

Hamideh Safi-Aghdam (H)

Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
VA Connecticut Healthcare System, Newington, USA.

Surbhi Pathania (S)

Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
VA Connecticut Healthcare System, Newington, USA.

Shariful Syed (S)

Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
VA Connecticut Healthcare System, Newington, USA.

Brian Pittman (B)

Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.

Deepak C D'Souza (DC)

Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
VA Connecticut Healthcare System, Newington, USA.

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Classifications MeSH