bioRxiv (Cold Spring Harbor Laboratory)
July 14, 2021
Galen Ballentine, Sam Friedman, Danilo Bzdok
6 citations
preprint
Psychedelic drugs alter consciousness by disrupting how the brain's higher association cortex processes incoming sensory signals. Analyzing 6,850 free-form testimonials about 27 drugs and linking them to 40 neurotransmitter receptor subtypes via gene transcription maps, a pattern-learning approach revealed that specific changes in awareness—such as dissolving self-world boundaries or fractal visual distortions—correspond to distinct distributions of receptor densities across the cortex. Ego-dissolution-like experiences were tied to 5-HT2A, D2, KOR, and NMDA receptors in both deep hierarchical (associative higher-order cortex) and shallow hierarchical (visual cortex) brain regions. Emotional effects involved 5-HT2A and Imidazoline1 receptors, while auditory and visual sensations involved SERT, 5-HT1A, and 5-HT2A receptors. Each receptor-experience factor spanned between higher-level association and sensory input poles, potentially relating to a collapse of hierarchical order among large-scale brain networks.
bioRxiv (Cold Spring Harbor Laboratory)
January 8, 2025
Delong Zhou, Heike Schuler, Vedrana Cvetkovska et al.
2 citations
preprint
A single dose of psilocybin increases synaptic transmission in the medial prefrontal cortex of mice. Single-cell RNA sequencing reveals that, 24 hours after administration, plasticity-related gene expression rises in excitatory neurons, with particularly robust changes in a deep-layer neuron type called L5/6 NP. This cell-type specificity aligns with 5-HT 2C receptor expression patterns, not 5-HT 2A. Multivariate analyses show that psilocybin-induced gene expression in L5/6 NP neurons predicts 5-HT 2C transcript levels. Blocking 5-HT 2C receptors with an antagonist attenuates the sustained effect on synaptic transmission, identifying 5-HT 2C signaling and L5/6 NP neurons as key mediators of psilocybin's lasting neuroplastic effects.
bioRxiv Preprint Server
June 7, 2026
Andrea I. Luppi, Dragana Manasova, Justine Y. Hansen et al.
preprint
Functional connectivity in the awake human brain is shaped primarily by cognitive co-activation—the tendency of brain regions to work together during mental tasks—more than by structural or molecular constraints. This predominance is systematically lost across five datasets involving pharmacological and pathological perturbations of consciousness (chronic disorders of consciousness; anesthesia with sevoflurane, propofol, or ketamine), when cognition is disconnected from the environment or abolished. During such states, the predictors of functional architecture shift away from cognitive co-activation and toward anatomical and molecular constraints.