Psychedelic 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.
Subanesthetic doses of ketamine, similar to those used in antidepressant studies, increase anterior theta and gamma power but decrease posterior theta, delta, and alpha power, as shown by magnetoencephalographic recordings. Dynamic causal modeling revealed a decrease in NMDA and AMPA-mediated frontal-to-parietal connectivity, with AMPA-mediated changes persisting up to 50 minutes after infusion ceased, even after perceptual distortions had ended. A decrease in gain of parietal pyramidal cells correlated with participants' self-reports of blissful state. These alterations in frontoparietal connectivity patterns may be important in generating the antidepressant response to ketamine.