Broadband Cortical Desynchronization Underlies the Human Psychedelic State
Matthew J. Brookes, David Errtizoe, Ben Sessa, Andreas Papadopoulos, Mark Bolstridge, Krish D. Singh, Amanda Feilding, Suresh Muthukumaraswamy, Robin Carhart‐Harris, Rosalyn Moran, Tom A. Williams, Karl Friston, David Nutt
Journal of Neuroscience September 18, 2013 DOI: 10.1523/jneurosci.2063-13.2013 via OpenAlex
Summary
AI-generated from the abstractPsychedelic drugs like psilocybin produce profound changes in consciousness by desynchronizing ongoing oscillatory rhythms in the cortex. Using magnetoencephalography in healthy participants, psilocybin reduced spontaneous cortical oscillatory power from 1 to 50 Hz in posterior association cortices and from 8 to 100 Hz in frontal association cortices, with large decreases in default-mode network areas. Low-level visually induced and motor-induced gamma-band oscillations were unaffected, suggesting some basic oscillatory activity is preserved. Dynamic causal modeling indicated that posterior cingulate cortex desynchronization results from increased excitability of deep-layer pyramidal neurons rich in 5-HT 2A receptors.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Healthy human participants |
| Intervention | Psilocybin |
| Topics | Default mode network Psilocybin |
| Keywords | Neuroscience Magnetoencephalography Posterior cingulate |
| Citations | 501 |
| Key finding | Psilocybin reduces spontaneous cortical oscillatory power across a wide frequency range in posterior and frontal association cortices, including default-mode network areas, while sparing low-level induced gamma oscillations, likely via 5-HT 2A receptor-mediated excitation of deep pyramidal neurons. |
Abstract
Psychedelic drugs produce profound changes in consciousness, but the underlying neurobiological mechanisms for this remain unclear. Spontaneous and induced oscillatory activity was recorded in healthy human participants with magnetoencephalography after intravenous infusion of psilocybin—prodrug of the nonselective serotonin 2A receptor agonist and classic psychedelic psilocin. Psilocybin reduced spontaneous cortical oscillatory power from 1 to 50 Hz in posterior association cortices, and from 8 to 100 Hz in frontal association cortices. Large decreases in oscillatory power were seen in areas of the default-mode network. Independent component analysis was used to identify a number of resting-state networks, and activity in these was similarly decreased after psilocybin. Psilocybin had no effect on low-level visually induced and motor-induced gamma-band oscillations, suggesting that some basic elements of oscillatory brain activity are relatively preserved during the psychedelic experience. Dynamic causal modeling revealed that posterior cingulate cortex desynchronization can be explained by increased excitability of deep-layer pyramidal neurons, which are known to be rich in 5-HT 2A receptors. These findings suggest that the subjective effects of psychedelics result from a desynchronization of ongoing oscillatory rhythms in the cortex, likely triggered by 5-HT 2A receptor-mediated excitation of deep pyramidal cells.