Psilocybin does not induce the vulnerability marker HSP70 in neurons susceptible to Olney’s lesions

S-ketamine, a N-methyl-D-aspartate receptor (NMDAR) antagonist, and psilocybin, a 5-hydroxy-tryptamine (serotonin) 2A receptor (5-HT2AR) agonist, are reported as effective rapid-acting antidepressants. Both compounds increase glutamate signalling and evoke cortical hyperexcitation. S-ketamine induce...

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Main Authors: Iorgu, Ana-Maria (Author) , Vasilescu, Andrei-Nicolae (Author) , Pfeiffer, Natascha (Author) , Spanagel, Rainer (Author) , Mallien, Anne Stephanie (Author) , Inta, Dragos (Author) , Gass, Peter (Author)
Format: Article (Journal)
Language:English
Published: 07 November 2023
In: European archives of psychiatry and clinical neuroscience
Year: 2024, Volume: 274, Issue: 4, Pages: 1013-1019
ISSN:1433-8491
DOI:10.1007/s00406-023-01699-3
Online Access:Verlag, kostenfrei, Volltext: https://doi.org/10.1007/s00406-023-01699-3
Verlag, kostenfrei, Volltext: https://link.springer.com/article/10.1007/s00406-023-01699-3
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Author Notes:Ana-Maria Iorgu, Andrei-Nicolae Vasilescu, Natascha Pfeiffer, Rainer Spanagel, Anne Stephanie Mallien, Dragos Inta, Peter Gass
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Summary:S-ketamine, a N-methyl-D-aspartate receptor (NMDAR) antagonist, and psilocybin, a 5-hydroxy-tryptamine (serotonin) 2A receptor (5-HT2AR) agonist, are reported as effective rapid-acting antidepressants. Both compounds increase glutamate signalling and evoke cortical hyperexcitation. S-ketamine induces neurotoxicity especially in the retrosplenial cortex (Olney’s lesions). Whether psilocybin produces similar neurotoxic effects has so far not been investigated. We performed an immunohistochemical whole-brain mapping for heat shock protein 70 (HSP70) in rats treated with psilocybin, S-ketamine, and MK-801. In contrast to S-ketamine- and MK-801-treated animals, we did not detect any HSP70-positive neurons in retrosplenial cortex of rats treated with psilocybin. Our results suggest that psilocybin might be safer for clinical use compared to S-ketamine regarding neuronal damage.
Item Description:Gesehen am 04.03.2024
Physical Description:Online Resource
ISSN:1433-8491
DOI:10.1007/s00406-023-01699-3