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Toxicology of Psychoactive Drugs
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Toxicology of Psychoactive Drugs

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 21 May 2025 | Viewed by 1538

Special Issue Editors

Dr. Sabrine Bilel

E-Mail Website
Guest Editor
Department of Translational Medicine, Forensic Toxicology Laboratory, LTTA Center, University of Ferrara, 44121 Ferrara, Italy
Interests: novel psychoactive substances; synthetic opioids; animal behavior; drug addiction; toxicology of NPS; respiratory depression; antidotes
Dr. Matteo Marti

E-Mail Website
Guest Editor
1. Department of Translational Medicine, LTTA Center and Center of Gender Medicine, University of Ferrara, 44121 Ferrara, Italy
2. Collaborative Center for Anti-Drug Policies Department, Presidency of the Council of Ministers, 44121 Ferrara, Italy
Interests: novel psychoactive substances; synthetic cannabinoids; cathinones; synthetic opioids; animal behavior; drug addiction; toxicology of nps; phenethylamines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Psychoactive drugs, including illicit drugs, therapeutic agents, and novel psychoactive substances, interact intricately with molecular targets of the central nervous system, and their use is often accompanied by adverse toxicological effects. At the molecular level, such effects involve complex interactions with neurotransmitter systems, receptors, enzymes, and intracellular pathways, leading to a cascade of biochemical and cellular disruptions. Despite advances in pharmacology, the precise mechanisms of toxicity of psychoactive substance exposure remain poorly understood.

This Special Issue aims to advance our understanding of the toxicological effects of psychoactive substances at the molecular level. We welcome original research and reviews that elucidate in vitro and in vivo studies with a focus on the effects and mechanisms of toxicity of these substances. This issue aims to foster a comprehensive understanding of the molecular underpinnings of psychoactive substance toxicity, paving the way for innovative therapeutic interventions and harm reduction strategies.

Dr. Sabrine Bilel
Dr. Matteo Marti
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • psychoactive substances
  • cannabis
  • synthetic cannabinoids
  • cathinones
  • synthetic opioids
  • toxicology
  • receptors
  • behavioral effects
  • antagonists
  • central nervous system

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Published Papers (3 papers)

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Research

16 pages, 1157 KiB  
Article
Halved Dose of Antipsychotics Versus High-Dose Antipsychotic Therapy for Relapse in Patients with Schizophrenia Receiving High-Dose Antipsychotic Therapy: A Randomized Single-Blind Trial
by Ryota Ataniya, Takeshi Koike and Atsuko Inamoto
Int. J. Mol. Sci. 2025, 26(9), 4003; https://doi.org/10.3390/ijms26094003 - 23 Apr 2025
Abstract
Both a shortage and an excess of dopamine (DA) in the prefrontal cortex and striatum result in their decreased functions, and the relationship between the DA levels and their functions exhibits an inverted-U shape. Increased DA transmission via dose reduction in the currently [...] Read more.
Both a shortage and an excess of dopamine (DA) in the prefrontal cortex and striatum result in their decreased functions, and the relationship between the DA levels and their functions exhibits an inverted-U shape. Increased DA transmission via dose reduction in the currently used antipsychotics may improve the activation of DA-related symptoms in schizophrenia; these include delusions and auditory hallucinations caused by increased DA release. In this case, reducing the dose of the antipsychotic may be a treatment option for relapse in patients with schizophrenia who are already on high doses of antipsychotics and find it difficult to further increase the dose. A total of 54 inpatients with schizophrenia receiving high-dose antipsychotic therapy were randomly assigned to either the halved-dose group or the high-dose group (symptomatic treatment). The study compared the time from relapse to improvement between the two groups. In the halved-dose group, the period until relapse improvement ranged from 1 to 3 weeks, while the high-dose group experienced improvement in 4 to 9 weeks, and a significant difference was observed between the two groups using Kaplan–Meier survival analysis (p < 0.001). Full article
(This article belongs to the Special Issue Toxicology of Psychoactive Drugs)
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18 pages, 2075 KiB  
Article
Acute Effects of the Psychedelic Phenethylamine 25I-NBOMe in C57BL/6J Male Mice
by Sabrine Bilel, Cristina Miliano, Giorgia Corli, Marta Bassi, Massimo Trusel, Raffaella Tonini, Maria Antonietta De Luca and Matteo Marti
Int. J. Mol. Sci. 2025, 26(6), 2815; https://doi.org/10.3390/ijms26062815 - 20 Mar 2025
Viewed by 478
Abstract
25I-NBOMe (4-Iodo-2,5-dimethoxy-N-(2-methoxybenzyl) phenethylamine) is a synthetic psychedelic compound abused for its ambiguous legal state as a counterfeit lysergic acid diethylamide (LSD). 25I-NBOMe acts as a selective agonist of 5HT2A receptors leading to hallucinations, intoxications, and fatalities. Here, we assessed the rewarding properties [...] Read more.
25I-NBOMe (4-Iodo-2,5-dimethoxy-N-(2-methoxybenzyl) phenethylamine) is a synthetic psychedelic compound abused for its ambiguous legal state as a counterfeit lysergic acid diethylamide (LSD). 25I-NBOMe acts as a selective agonist of 5HT2A receptors leading to hallucinations, intoxications, and fatalities. Here, we assessed the rewarding properties of 25I-NBOMe and its behavioral and neurotoxic acute effects on the central nervous system of C57BL/6J mice. We evaluated the dopamine (DA) levels using in vivo microdialysis in the nucleus accumbens (NAc) shell after 25I-NBOMe (0.1–1 mg/kg i.p.) injection. We also investigated the effects of 25I-NBOMe (0.1–1 mg/kg i.p.) on locomotor activity, reaction time, and prepulse inhibition. Moreover, we assessed the acute 25I-NBOMe (1 µM) effects on synaptic transmission and plasticity in the medial prefrontal cortex (mPFC) by using ex vivo electrophysiology. Our findings suggest that 25I-NBOMe affects the DA transmission in NAc shell at the highest dose tested, increases the reaction time within 30 min after the administration, and disrupts the PPI. In slices, it prevents long-term synaptic potentiation (LTP) in the mPFC, an effect that could not be reverted by the co-administration of the selective 5HT2A antagonist (MDL100907). Overall, these findings provide valuable new insights into the effects of 25I-NBOMe and the associated risks of its use. Full article
(This article belongs to the Special Issue Toxicology of Psychoactive Drugs)
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25 pages, 11452 KiB  
Article
Methamphetamine and Methamphetamine-Induced Neuronal Exosomes Modulate the Activity of Rab7a via PTEN to Exert an Influence on the Disordered Autophagic Flux Induced in Neurons
by Hai Qiu, Manting Zhang, Minchun Li, Chuanxiang Chen, Huijun Wang and Xia Yue
Int. J. Mol. Sci. 2025, 26(6), 2644; https://doi.org/10.3390/ijms26062644 - 14 Mar 2025
Viewed by 473
Abstract
Autophagy is a critical mechanism by which methamphetamine (METH) induces neuronal damage and neurotoxicity. Prolonged METH exposure can result in the accumulation of autophagosomes within cells. The autophagy process encompasses several essential vesicle-related biological steps, collectively referred to as the autophagic flux. However, [...] Read more.
Autophagy is a critical mechanism by which methamphetamine (METH) induces neuronal damage and neurotoxicity. Prolonged METH exposure can result in the accumulation of autophagosomes within cells. The autophagy process encompasses several essential vesicle-related biological steps, collectively referred to as the autophagic flux. However, the precise mechanisms by which METH modulates the autophagic flux and the underlying pathways remain to be elucidated. In this study, we utilized a chronic METH exposure mouse model and cell model to demonstrate that METH treatment leads to an increase in p62 and LC3B-II and the accumulation of autophagosomes in striatal neurons and SH-SY5Y cells. To assess autophagic flux, this study utilized autophagy inhibitors and inducers. The results demonstrated that the lysosomal inhibitor chloroquine exacerbated autophagosome accumulation; however, blocking autophagosome formation with 3-methyladenine did not prevent METH-induced autophagosome accumulation. Compared to the autophagy activator rapamycin, METH significantly reduced autophagosome–lysosome fusion, leading to autophagosome accumulation. Rab7a is a critical regulator of autophagosome–lysosome fusion. Although Rab7a expression was upregulated in SH-SY5Y cells and brain tissues after METH treatment, immunoprecipitation experiments revealed weakened interactions between Rab7a and the lysosomal protein RILP. Overexpression of active Rab7a (Rab7a Q67L) significantly alleviated the METH-induced upregulation of LC3-II and p62. PTEN, a key regulator of Rab7a dephosphorylation, was downregulated following METH treatment, resulting in decreased Rab7a dephosphorylation and reduced Rab7a activity, thereby contributing to autophagosome accumulation. We further investigated the role of neuronal exosomes in the autophagy process. Our results demonstrated that the miRNA expression profiles in exosomes released by METH-induced SH-SY5Y cells were significantly altered, with 122 miRNAs upregulated and 151 miRNAs downregulated. KEGG and GO enrichment analyses of these differentially expressed miRNAs and their target genes revealed significant associations with the autophagy pathway and potential regulation of PTEN expression. Our experiments confirmed that METH-induced exosomes reduced PTEN expression levels and decreased Rab7a dephosphorylation, thereby exacerbating autophagic flux impairment and autophagosome accumulation. In conclusion, our study indicated that METH and its induced neuronal exosomes downregulate PTEN expression, leading to reduced Rab7a dephosphorylation. This, in turn, hinders the fusion of autophagosomes and lysosomes, ultimately resulting in autophagic flux impairment and neuronal damage. Full article
(This article belongs to the Special Issue Toxicology of Psychoactive Drugs)
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