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
November 13, 2014
Anna Górska, Krystyna Gołembiowska
36 citations
Caffeine worsens the increase in dopamine and serotonin release caused by MDMA (ecstasy) in the mouse striatum. Blocking adenosine A1 or A2A receptors with selective antagonists mimics caffeine's effect, with the A2A antagonist being more potent. This suggests that caffeine exacerbates MDMA's neurochemical effects and potential toxicity through adenosine receptor blockade, not through monoamine oxidase inhibition.
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.
Neurotoxicity Research
July 1, 2017
Jana Ruda-Kucerova, Zuzana Babinska, Tibor Stark et al.
26 citations
In a rat model of schizophrenia (MAM-treated rats), ketamine reduced methamphetamine self-administration in control animals but not in MAM-treated animals. MAM rats showed a lack of habituation in locomotor activity but maintained stable methamphetamine intake similar to controls. Ketamine's effect may stem from increased glutamatergic signaling in the prefrontal cortex via NMDA receptor antagonism and disinhibition of GABA interneurons, a mechanism impaired in MAM rats. This suggests ketamine's anti-craving potential in clinical settings, though it may be ineffective in schizophrenia.
Neurotoxicity Research
July 26, 2016
Karolina Noworyta, Katarzyna Kamińska, Grzegorz Kreiner et al.
26 citations
The hallucinogen 5-MeO-DIPT ('foxy') increases dopamine, serotonin, and glutamate release in rat brain regions including the striatum, nucleus accumbens, and frontal cortex, with varying potency. It raises serotonin and lowers its metabolite 5-HIAA in tissue, likely by inhibiting the serotonin transporter. Decreases in dopamine and its metabolites suggest possible damage to dopamine terminals or adaptive changes in turnover. DNA strand breaks persisted for up to 60 days, indicating marked neurotoxicity. The drug also induced head-twitch responses and potentiated forepaw treading, suggesting its hallucinogenic effects involve stimulation of 5-HT2A and 5-HT1A receptors.
Neurotoxicity Research
June 7, 2025
Felype Valentim Duarte Castelhano, Carolina Aparecida de Faria Almeida, Giulia de Assis Braz et al.
3 citations
Combining ketamine with ethanol triggers greater nerve cell death than either drug alone, acting through oxidative stress and two programmed-cell-death pathways. In human neuroblastoma cells, the lowest observed adverse-effect levels were 1 mM ketamine and 100 mM ethanol. After 48 hours, the combination produced a possible synergistic increase in late apoptotic cells. Glutathione levels fell within 6 hours, and glutathione-peroxidase activity rose in all groups. Only the combination increased glutathione reductase and glutathione S-transferase activities after 3 hours, along with elevated caspase-8 and Bax expression, signaling both extrinsic and intrinsic apoptosis. The findings suggest heightened neuronal damage risk from combined use, though limitations include enzyme-activity variability, reduced sample size for some markers, and use of an immortalized cell line.
Neurotoxicity Research
October 1, 2022
Asieh Hosseini, Seyed Mohammad-Hossein Shetab-Boushehri, Seyed Vahid Shetab-Boushehri
3 citations
Methamphetamine (MA) and MDMA show stronger cytotoxic effects on neuronal and glial cells. MDMA causes more potent mitochondrial toxicity and stronger necrotic and autophagic effects than MA in both cell lines. While MDMA induces a stronger apoptotic effect than MA in glial cells, both drugs have equal apoptotic effects on neuronal cells. MDMA also produces greater mitochondrial toxicity and stronger necrotic, apoptotic, and autophagic effects in neuronal cells compared to glial cells.
Neurotoxicity Research
May 1, 2019
Peng Xu, Qiyang Qiu, Haijie Li et al.
25C-NBOMe, a high-potency psychedelic acting on the 5-HT2A receptor, reduced cell viability in SH-SY5Y, PC12, and SN4741 cells with IC50 values of 89, 78, and 62 μM, respectively. Methamphetamine reduced viability at millimolar IC50 values in the same tests, making 25C-NBOMe over 50 times more potent than methamphetamine in reducing SH-SY5Y cell viability. 25C-NBOMe increased phosphorylated ERK expression and decreased phosphorylated Akt and phosphorylated Ser9-GSK3β. GSK3β inhibitors or MEK inhibitors prevented 25C-NBOMe-induced neurotoxicity, suggesting inhibition of the Akt pathway and activation of the ERK cascade are involved.
Neurotoxicity Research
November 1, 2016
Patrycja Kleczkowska, Irena Smaga, Malgorzata Filip et al.
Cannabinoids, despite their illegal status, have recognized therapeutic potential and are often used recreationally by young adults, sometimes as an alternative to other drugs or to enhance pleasure. They are frequently taken alongside medications for alcohol use disorder (AUD) and alcohol withdrawal syndrome (AWS), such as disulfiram, acamprosate, and naltrexone. This paper reviews recent findings on possible beneficial effects and interactions between cannabinoids and these AUD/AWS medications, whether the conditions are comorbid or separate.
Neurotoxicity Research
April 1, 2016
Krystyna Gołembiowska, Alexandra Jurczak, Katarzyna Kamińska et al.
New psychoactive designer drugs like PMA, PMMA, and mephedrone, which are used as substitutes in ecstasy pills, increase the release of dopamine and serotonin in rat brain regions including the striatum, nucleus accumbens, and frontal cortex, similar to MDMA. The drugs also altered tissue levels of these neurotransmitters in region-specific ways: for example, mephedrone and PMMA increased dopamine in the striatum, while mephedrone and PMMA decreased dopamine in the frontal cortex. These changes suggest the drugs may have dependence potential, though further research is needed to assess neurotoxicity and abuse risk.