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      Neuronal and peripheral damages induced by synthetic psychoactive substances: an update of recent findings from human and animal studies

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          Abstract

          Preclinical and clinical studies indicate that synthetic psychoactive substances, in addition to having abuse potential, may elicit toxic effects of varying severity at the peripheral and central levels. Nowadays, toxicity induced by synthetic psychoactive substances poses a serious harm for health, since recreational use of these substances is on the rise among young and adult people. The present review summarizes recent findings on the peripheral and central toxicity elicited by “old” and “new” synthetic psychoactive substances in humans and experimental animals, focusing on amphetamine derivatives, hallucinogen and dissociative drugs and synthetic cannabinoids.

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          The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy").

          Douglas R. Green, Esther O'Shea, David J. Elliott … (2003)
          The amphetamine derivative (+/-)-3,4-methylenedioxymethamphetamine (MDMA, ecstasy) is a popular recreational drug among young people, particularly those involved in the dance culture. MDMA produces an acute, rapid enhancement in the release of both serotonin (5-HT) and dopamine from nerve endings in the brains of experimental animals. It produces increased locomotor activity and the serotonin behavioral syndrome in rats. Crucially, it produces dose-dependent hyperthermia that is potentially fatal in rodents, primates, and humans. Some recovery of 5-HT stores can be seen within 24 h of MDMA administration. However, cerebral 5-HT concentrations then decline due to specific neurotoxic damage to 5-HT nerve endings in the forebrain. This neurodegeneration, which has been demonstrated both biochemically and histologically, lasts for months in rats and years in primates. In general, other neurotransmitters appear unaffected. In contrast, MDMA produces a selective long-term loss of dopamine nerve endings in mice. Studies on the mechanisms involved in the neurotoxicity in both rats and mice implicate the formation of tissue-damaging free radicals. Increased free radical formation may result from the further breakdown of MDMA metabolic products. Evidence for the occurrence of MDMA-induced neurotoxic damage in human users remains equivocal, although some biochemical and functional data suggest that damage may occur in the brains of heavy users. There is also some evidence for long-term physiological and psychological changes occurring in human recreational users. However, such evidence is complicated by the lack of knowledge of doses ingested and the fact that many subjects studied are or have been poly-drug users.
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            Methamphetamine toxicity and messengers of death.

            Irina N. Krasnova, Jean Lud Cadet (2009)
            Methamphetamine (METH) is an illicit psychostimulant that is widely abused in the world. Several lines of evidence suggest that chronic METH abuse leads to neurodegenerative changes in the human brain. These include damage to dopamine and serotonin axons, loss of gray matter accompanied by hypertrophy of the white matter and microgliosis in different brain areas. In the present review, we summarize data on the animal models of METH neurotoxicity which include degeneration of monoaminergic terminals and neuronal apoptosis. In addition, we discuss molecular and cellular bases of METH-induced neuropathologies. The accumulated evidence indicates that multiple events, including oxidative stress, excitotoxicity, hyperthermia, neuroinflammatory responses, mitochondrial dysfunction, and endoplasmic reticulum stress converge to mediate METH-induced terminal degeneration and neuronal apoptosis. When taken together, these findings suggest that pharmacological strategies geared towards the prevention and treatment of the deleterious effects of this drug will need to attack the various pathways that form the substrates of METH toxicity.
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              Multiple receptors contribute to the behavioral effects of indoleamine hallucinogens.

              Adam Halberstadt, Mark A. Geyer (2011)
              Serotonergic hallucinogens produce profound changes in perception, mood, and cognition. These drugs include phenylalkylamines such as mescaline and 2,5-dimethoxy-4-methylamphetamine (DOM), and indoleamines such as (+)-lysergic acid diethylamide (LSD) and psilocybin. Despite their differences in chemical structure, the two classes of hallucinogens produce remarkably similar subjective effects in humans, and induce cross-tolerance. The phenylalkylamine hallucinogens are selective 5-HT(2) receptor agonists, whereas the indoleamines are relatively non-selective for serotonin (5-HT) receptors. There is extensive evidence, from both animal and human studies, that the characteristic effects of hallucinogens are mediated by interactions with the 5-HT(2A) receptor. Nevertheless, there is also evidence that interactions with other receptor sites contribute to the psychopharmacological and behavioral effects of the indoleamine hallucinogens. This article reviews the evidence demonstrating that the effects of indoleamine hallucinogens in a variety of animal behavioral paradigms are mediated by both 5-HT(2) and non-5-HT(2) receptors.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neural Regen Res
                Journal ID (iso-abbrev): Neural Regen Res
                Journal ID (publisher-id): NRR
                Title: Neural Regeneration Research
                Publisher: Wolters Kluwer - Medknow (India )
                ISSN (Print): 1673-5374
                ISSN (Electronic): 1876-7958
                Publication date Collection: May 2020
                Publication date (Electronic): 08 November 2019
                Volume: 15
                Issue: 5
                Pages: 802-816
                Affiliations
                [1 ]Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy
                [2 ]National Institute of Neuroscience (INN), University of Cagliari, Cagliari, Italy
                [3 ]National Research Council of Italy, Institute of Neuroscience, Cagliari, Italy
                Author notes
                [* ] Correspondence to: Nicola Simola, nicola.simola@ 123456unica.it or nicola.simola@ 123456gmail.com .

                Author contributions: All authors wrote the manuscript. NS approved the final manuscript.

                Author information
                http://orcid.org/0000-0001-7296-3197
                Article
                Publisher ID: NRR-15-802
                DOI: 10.4103/1673-5374.268895
                PMC ID: 6990793
                PubMed ID: 31719240
                SO-VID: 8b0f0252-6a44-404d-8da2-146d28e4a61a
                Copyright © Copyright: © Neural Regeneration Research
                License:

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                Date received : 01 July 2019
                Date revision received : 03 July 2019
                Date accepted : 30 July 2019
                Categories
                Subject: Review

                Keywords: cannabinoids,dissociatives,hallucinogens,ketamine,mdma,methamphetamine,methoxetamine,neuroinflammation,neurotoxicity,nps
                Data availability:
                Keywords: cannabinoids, dissociatives, hallucinogens, ketamine, mdma, methamphetamine, methoxetamine, neuroinflammation, neurotoxicity, nps

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