The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Psychedelics promote neuroplasticity through the activation of intracellular 5-HT2A receptors
Open accessAbstract
Decreased dendritic spine density in the cortex is a hallmark of several neuropsychiatric diseases, and the ability to promote cortical neuron growth has been hypothesized to underlie the rapid and sustained therapeutic effects of psychedelics. Activation of 5-hydroxytryptamine (serotonin) 2A receptors (5-HT2ARs) is essential for psychedelic-induced cortical plasticity, but it is currently unclear why some 5-HT2AR agonists promote neuroplasticity, whereas others do not. We used molecular and genetic tools to demonstrate that intracellular 5-HT2ARs mediate the plasticity-promoting properties of psychedelics; these results explain why serotonin does not engage similar plasticity mechanisms. This work emphasizes the role of location bias in 5-HT2AR signaling, identifies intracellular 5-HT2ARs as a therapeutic target, and raises the intriguing possibility that serotonin might not be the endogenous ligand for intracellular 5-HT2ARs in the cortex.
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Cites
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Psychedelics promote structural and functional neural plasticity
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Antidepressant drugs act by directly binding to TRKB neurotrophin receptors
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Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation
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Psilocybin induces rapid and persistent growth of dendritic spines in frontal cortex in vivo
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Psilocybin induces rapid and persistent growth of dendritic spines in frontal cortex in vivo
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Research works printed but not linked: 2
- 10.1161/01.RES.70.6.1320 · doi:10.1161/01.res.70.6.1320
- 10.1016/0304-3940(86)90534-3 · doi:10.1016/0304-3940(86)90534-3
Cited by
Psychedelics reopen the social reward learning critical period
Nardou, R., Sawyer, E., Song, Y. J., Wilkinson, M., Padovan-Hernandez, Y., de Deus, J. L., Wright, N., Lama, C., Faltin, S., Goff, L. A., et al. (2023) · Nature · doi:10.1038/s41586-023-06204-3 · Cited by 358
Mechanisms of SSRI Therapy and Discontinuation
Sharp, T., & Collins, H. (2023) · Current Topics in Behavioral Neurosciences · doi:10.1007/7854_2023_452 · Cited by 55
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“…serotonin and has agonistic properties at a variety of serotonin receptors (mainly 5-HT2A, 5-HT2C, 5-HT1A), but also glutamate, dopamine, acetylcholine, sigma-1, and trace amine-associated receptors (9–12), similar to other psychedelics such as psilocybin or lysergic acid diethylamide (LSD) (13).”
BackgroundRethinking the role of TRKB in the action of antidepressants and psychedelics
Brunello, C. A., Cannarozzo, C., & Castrén, E. (2024) · Trends in Neurosciences · doi:10.1016/j.tins.2024.08.011 · Cited by 31
Serotonergic neuromodulation of synaptic plasticity
Higa, G. S. V., Viana, F. J. C., Francis-Oliveira, J., Cruvinel, E., Franchin, T. S., Marcourakis, T., Ulrich, H., & De Pasquale, R. (2024) · Neuropharmacology · doi:10.1016/j.neuropharm.2024.110036 · Cited by 29
Metadata
- Authors
- Vargas, M. V., Dunlap, L. E., Dong, C., Carter, S. J., Tombari, R. J., Jami, S. A., Cameron, L. P., Patel, S. D., Hennessey, J. J., Saeger, H. N., McCorvy, J. D., Gray, J. A., Tian, L., & Olson, D. E.
- Venue
- Science
- Published
- 2023-02-17
- Volume
- 379
- Issue
- 6633
- Pages
- 700-706
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W4321033185
- Cited by
- 489
- References
- 57
- FWCI
- 134.11
- Type
- journal article
- Language
- en
- Open access
- green
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- Vargas, M. V., Dunlap, L. E., Dong, C., Carter, S. J., Tombari, R. J., Jami, S. A., Cameron, L. P., Patel, S. D., Hennessey, J. J., Saeger, H. N., McCorvy, J. D., Gray, J. A., Tian, L., & Olson, D. E. (2023). Psychedelics promote neuroplasticity through the activation of intracellular 5-HT2A receptors. Science. https://doi.org/10.1126/science.adf0435
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
