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      Recent Advances in Methamphetamine Neurotoxicity Mechanisms and Its Molecular Pathophysiology

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Methamphetamine (METH) is a sympathomimetic amine that belongs to phenethylamine and amphetamine class of psychoactive drugs, which are widely abused for their stimulant, euphoric, empathogenic, and hallucinogenic properties. Many of these effects result from acute increases in dopamine and serotonin neurotransmission. Subsequent to these acute effects, METH produces persistent damage to dopamine and serotonin release in nerve terminals, gliosis, and apoptosis. This review summarized the numerous interdependent mechanisms including excessive dopamine, ubiquitin-proteasome system dysfunction, protein nitration, endoplasmic reticulum stress, p53 expression, inflammatory molecular, D 3 receptor, microtubule deacetylation, and HIV-1 Tat protein that have been demonstrated to contribute to this damage. In addition, the feasible therapeutic strategies according to recent studies were also summarized ranging from drug and protein to gene level.

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          The endocannabinoid system and the brain.

          Raphael Mechoulam, Linda A. Parker (2013)
          The psychoactive constituent in cannabis, Δ(9)-tetrahydrocannabinol (THC), was isolated in the mid-1960s, but the cannabinoid receptors, CB1 and CB2, and the major endogenous cannabinoids (anandamide and 2-arachidonoyl glycerol) were identified only 20 to 25 years later. The cannabinoid system affects both central nervous system (CNS) and peripheral processes. In this review, we have tried to summarize research--with an emphasis on recent publications--on the actions of the endocannabinoid system on anxiety, depression, neurogenesis, reward, cognition, learning, and memory. The effects are at times biphasic--lower doses causing effects opposite to those seen at high doses. Recently, numerous endocannabinoid-like compounds have been identified in the brain. Only a few have been investigated for their CNS activity, and future investigations on their action may throw light on a wide spectrum of brain functions.
          Article 0 comments Cited 300 times – based on 0 reviews     Review now
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            Reactive astrocytes: cellular and molecular cues to biological function.

            J.L. Ridet, A. Privat, S.K. Malhotra … (1997)
            For several decades, the reactive gliosis that occurs after an injury to the CNS has been considered one of the major impediments to axonal regeneration. Nevertheless, recent studies have suggested that in certain conditions, reactive astrocytes may provide a permissive substratum to support axonal regrowth. The important criteria, allowing for the distinction between permissive and non-permissive gliosis, are the ultrastructural 3D organization of the scar and more importantly the recognition molecules expressed by reactive astrocytes. Reactive astrocytes express surface molecules and produce various neurotrophic factors and cytokines. The latter in turn might modulate the production of recognition molecules by reactive astrocytes, allowing them to support post-lesional axonal regrowth. Although numerous recent articles have focused on cytokines and cell adhesion molecules, scant attention has been paid to reactive astrocytes. Reactive astrocytes should be considered a key element, like neurons, of a dynamic environment, thus forming with neurons a functional unit involved in homeostasis, plasticity and neurotransmission. Attempts are in progress to identify molecular markers for reactive astrocytes.
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              Minocycline inhibits cytochrome c release and delays progression of amyotrophic lateral sclerosis in mice.

              D. Wu, Victor-Dan Ona, Hua Liu … (2002)
              Minocycline mediates neuroprotection in experimental models of neurodegeneration. It inhibits the activity of caspase-1, caspase-3, inducible form of nitric oxide synthetase (iNOS) and p38 mitogen-activated protein kinase (MAPK). Although minocycline does not directly inhibit these enzymes, the effects may result from interference with upstream mechanisms resulting in their secondary activation. Because the above-mentioned factors are important in amyotrophic lateral sclerosis (ALS), we tested minocycline in mice with ALS. Here we report that minocycline delays disease onset and extends survival in ALS mice. Given the broad efficacy of minocycline, understanding its mechanisms of action is of great importance. We find that minocycline inhibits mitochondrial permeability-transition-mediated cytochrome c release. Minocycline-mediated inhibition of cytochrome c release is demonstrated in vivo, in cells, and in isolated mitochondria. Understanding the mechanism of action of minocycline will assist in the development and testing of more powerful and effective analogues. Because of the safety record of minocycline, and its ability to penetrate the blood-brain barrier, this drug may be a novel therapy for ALS.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Behav Neurol
                Journal ID (iso-abbrev): Behav Neurol
                Journal ID (publisher-id): BN
                Title: Behavioural Neurology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0953-4180
                ISSN (Electronic): 1875-8584
                Publication date (Print): 2015
                Publication date (Electronic): 12 March 2015
                Volume: 2015
                Electronic Location Identifier: 103969
                Affiliations
                1Department of Neurology, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China
                2Department of Neurology, Hospitals of The Armed Police Forces in Hebei, Shijiazhuang 050051, China
                Author notes

                Academic Editor: Antonio Pisani

                Article
                DOI: 10.1155/2015/103969
                PMC ID: 4377385
                PubMed ID: 25861156
                SO-VID: 96da4ba0-7d2a-4333-b79e-78548a31ffb1
                Copyright © Copyright © 2015 Shaobin Yu et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 9 January 2015
                Date revision received : 5 March 2015
                Date accepted : 5 March 2015
                Categories
                Subject: Review Article

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