Cluster 2
How It Works
5 articles
Neuroplasticity, BDNF, and the Default Mode Network
The hypothesis that psilocybin produces lasting change by reshaping neural connections and quieting the default mode network. The preclinical evidence is genuinely strong; the human, microdose-level evidence is thin — and keeping those apart is the whole point.
Updated Jun 4, 2026
Pharmacology Overview: How Psilocybin Acts in the Brain
How psilocybin works at the receptor level — prodrug conversion to psilocin, 5-HT2A agonism, default mode network modulation, and neuroplasticity — and the line between a well-characterized mechanism and a demonstrated microdose effect.
Updated Jun 4, 2026
Psilocybin to Psilocin: The Pharmacokinetics of a Prodrug
Psilocybin is inactive until the body converts it to psilocin. How that conversion works, how psilocin is absorbed, distributed, and cleared, why its short half-life shapes the practice of microdosing, and why dose-by-weight is an imperfect proxy for what reaches the brain.
Updated Jun 4, 2026
The 5-HT2A Mechanism: How Psilocin Engages the Serotonin System
Psilocin acts mainly as an agonist at the serotonin 5-HT2A receptor — the interaction at the centre of psychedelic pharmacology. What that means, the human evidence that it is causal, the role of 5-HT1A, and why full-dose receptor data don't settle what a microdose does.
Updated Jun 4, 2026
What the Mechanism Does and Doesn't Show
The cluster's reasoning capstone. A coherent pharmacological mechanism makes microdosing plausible; it cannot, by itself, demonstrate that a sub-perceptual dose works in humans. Why mechanism is not efficacy, full-dose is not microdose, and reports are not outcomes — and what evidence would actually settle the question.
Updated Jun 4, 2026