Ly · Cell reports 2018 · preclinical in vitro and in vivo laboratory experiment · n=?

Psychedelics Promote Structural and Functional Neural Plasticity.

Cited 1192 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Preclinical in vitro and in vivo laboratory study with no human data.

PubMed 29898390 · doi:10.1016/j.celrep.2018.05.022 · record verified 2026-08-28

What was done

Researchers evaluated the capacity of serotonergic psychedelics to induce structural and functional neural plasticity compared to ketamine. Using both in vitro cell cultures and in vivo animal models, they assessed neuritogenesis and spinogenesis in prefrontal cortex neurons. Synapse number and synaptic function were measured using fluorescence microscopy and electrophysiology. In addition, the study evaluated the role of TrkB, mTOR, and 5-HT2A signaling pathways in mediating these structural changes.

What was found

Serotonergic psychedelics promoted neuritogenesis and spinogenesis across in vitro and in vivo preparations. These morphological modifications were accompanied by increases in synapse count and functional synaptic activity. The structural plasticity was mechanistically linked to activation of the TrkB, mTOR, and 5-HT2A signaling pathways. The abstract reports directional findings only and does not provide exact numerical effect sizes, sample counts, or statistical values.

Why it matters

This study demonstrates that classic psychedelics share ketamine's ability to rapidly induce structural and functional neuroplasticity in the prefrontal cortex. It identifies specific intracellular signaling pathways mediating these effects, offering a mechanistic explanation for their potential antidepressant action and providing scaffolds for neuropsychiatric drug design.

Limits

The work is strictly preclinical, relying on cell culture and animal models rather than human clinical participants. The abstract does not specify the animal species, exact sample sizes, specific psychedelic compounds tested, dosing regimens, or quantitative outcome metrics. Findings cannot be directly translated to clinical efficacy or safety in patients with depression without human trial validation.

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