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
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.