International Journal of Molecular Sciences
June 16, 2022
Adam Wojtas, Agnieszka Bysiek, Agnieszka Wawrzczak‐bargieła et al.
110 citations
Ketamine and psilocybin, both fast-acting antidepressants in clinical studies, increase extracellular levels of dopamine, serotonin, glutamate, and GABA in the rat frontal cortex. Psilocybin also raises GABA in the reticular nucleus of the thalamus. However, both drugs cause oxidative DNA damage—psilocybin in the frontal cortex and both drugs in the hippocampus. Psilocybin at 10 mg/kg increases NR2A glutamate receptor subunit levels. Behavioral tests 24 hours after administration show no antidepressant or anxiolytic effects; only ketamine reduces locomotor activity. The observed neurotransmitter changes may lead to genotoxicity and altered receptor levels without markedly affecting behavior.
Neurotoxicity Research
April 15, 2019
Monika Herian, Adam Wojtas, Katarzyna Kamińska et al.
44 citations
25I-NBOMe, a synthetic hallucinogen related to the 2C family, increases extracellular levels of dopamine, serotonin, and glutamate in the rat frontal cortex, as measured by microdialysis in freely moving animals. It also raises tissue content of serotonin and its metabolite 5-HIAA but does not affect tissue dopamine or its metabolites. The drug elicits head-twitch response in rats, a behavioral marker of hallucinogenic effect in humans. Dose-response curves were inverted U-shaped for dopamine and serotonin release, but U-shaped for glutamate release and head-twitch response. The findings suggest that the hallucinogenic activity of 25I-NBOMe is linked to increased extracellular glutamate mediated by cortical 5-HT2A receptors, with modulation by 5-HT2C and 5-HT1A receptors.
Neurotoxicity Research
December 18, 2020
Adam Wojtas, Monika Herian, Mateusz Skawski et al.
33 citations
The hallucinogen 25B-NBOMe, which binds strongly to serotonin receptors, increased dopamine, serotonin, and glutamate release in the rat frontal cortex, striatum, and nucleus accumbens. It induced hallucinogenic activity, impaired short-term memory as measured by the novel object recognition test, and reduced locomotor activity in the open field test. In the light/dark box, rats spent more time in the dark zone, suggesting an anxiogenic effect. Scopolamine blocked the memory impairment. Unlike MDMA, 25B-NBOMe showed a subtle genotoxic effect in the comet assay. The changes in neurotransmitter levels may stem from its affinity for the 5-HT2A receptor.
Psychopharmacology
May 25, 2021
Monika Herian, Mateusz Skawski, Adam Wojtas et al.
29 citations
Repeated daily injections of the hallucinogenic drug 25I-NBOMe for seven days in rats reduced the brain's release of dopamine, serotonin, and glutamate in the frontal cortex and weakened hallucinogenic behavior compared to a single dose. In contrast, dopamine and serotonin release increased in the striatum and nucleus accumbens, and acetylcholine release rose across all brain regions. Chronic treatment also reduced motor activity, impaired short-term memory, and induced anxiety. These findings indicate that repeated use of 25I-NBOMe produces tolerance to its hallucinogenic effects while altering multiple neurotransmitter systems, with complex effects on memory, movement, and anxiety.
Pharmacological reports : PR
December 1, 2020
Monika Herian, Adam Wojtas, Małgorzata Katarzyna Sobocińska et al.
19 citations
The hallucinogenic compound 25I-NBOMe acts through specific serotonin receptors to produce its effects. In rats, blocking the 5-HT2A or 5-HT2C receptors with selective antagonists reduced both the hallucinogenic-like behavior (wet dog shakes) and the release of glutamate, dopamine, and serotonin in the frontal cortex caused by 25I-NBOMe. Blocking the 5-HT1A receptor did not affect the behavior or glutamate release but did decrease dopamine and serotonin release, likely by disinhibiting GABA neurons. These findings indicate that 5-HT2A and 5-HT2C receptors are key mediators of 25I-NBOMe's hallucinogenic activity and its effects on neurotransmitter release in the frontal cortex.
Scientific reports
February 21, 2022
Monika Herian, Adam Wojtas, Marzena Maćkowiak et al.
15 citations
The synthetic hallucinogen 25I-NBOMe crosses the blood-brain barrier easily and accumulates in the brain after repeated doses. In rats, chronic treatment caused DNA damage in brain tissue 72 hours later, but no signs of apoptosis. The number of glial cells decreased in the frontal and medial prefrontal cortex, while neural cells were unaffected. These findings suggest that oxidative DNA damage from 25I-NBOMe may lead to glial cell death, indicating potential brain toxicity from recreational use.
Critical reviews in toxicology
January 1, 2023
Monika Herian, Paweł Świt
9 citations
Hallucinogenic therapies show promise for neuropsychiatric disorders, but new psychoactive substances (NPS) like 25X-NBOMes—synthetic compounds with strong hallucinogenic properties—pose high toxicity risks. 25X-NBOMes bind strongly to serotonin, dopamine, adrenergic, and histamine receptors, causing severe intoxications and deaths. In humans, common side effects include tachycardia, anxiety, hypertension, and seizures. Preclinical studies confirm developmental impairments, cytotoxicity, cardiovascular toxicity, and behavioral changes. Their complex metabolism, involving many pathways, may explain the high toxicity. This review summarizes current knowledge about 25X-NBOMes, focusing on toxicity.
Neuropharmacology
December 1, 2023
Adam Wojtas, Monika Herian, Marzena Maćkowiak et al.
6 citations
Repeated administration of the hallucinogenic drug 25B-NBOMe (0.3 mg/kg for 7 days) in rats rapidly produced tolerance to its effects on neurotransmitter release and hallucinogenic behavior, as measured by the Wet Dog Shake test. The drug reduced dopamine, serotonin, and glutamate responses in the frontal cortex, striatum, and nucleus accumbens after a challenge dose. Genotoxicity, indicated by DNA damage, was found in the frontal cortex and hippocampus, with increased glial cells in cortical regions but no neuronal loss. Anxiety effects depended on treatment and environmental context, with anxiogenic effects observed after both single and repeated dosing.