Neuronal mitochondrial trafficking impairment : the cause or a consequence of neuronal dysfunction caused by amphetamine-like drugs
Joint Authors
Barbosa, Daniel Jose
Serrat, Roman
Ferreira, Luısa Maria
Branco, Paula Serio
Capela, Joao Paulo
Soriano, Eduardo
Carvalho, Felix
Bastos, Maria de Lourdes
Source
Journal of Drug and Alcohol Research
Publisher
Publication Date
2014-12-31
Country of Publication
Egypt
No. of Pages
7
Main Subjects
English Abstract
Drugs of abuse cause a variety of complex neuronal events at the cellular level, including changes in membrane excitability and neurotransmission, activation of complex signaling pathways, altered synaptic physiology and structural changes, and drug-evoked synaptic plasticity and neurotoxicity, which mediate both acuteand long-lasting effects and addiction.
Neuronal mitochondria are highly dynamic organelles that, by undergoing fusion and fission events, are efficiently translocated along the neuronal processes, frequently changing direction, pausing or switching to persistent docking.
The neuronal integrity and functionality are dependent upon the proper maintenance of a healthy mitochondrial population and their efficient distribution.
There is a general consensus that mitochondrial-dependent pathways can provide a major understanding concerning pathological processes underlying neurotoxicity of drugs of abuse.
As such, it is plausible to consider that alterations on mitochondrial trafficking may be key players on the neuronal effects mediated by these drugs.
This work aims to provide a comprehensive and up-to-date review of the data linking mitochondrial trafficking impairment to amphetamine-like drugs, and, thus, contribute to a better understanding of their neuronal effects.
Additionally, new research data describing alterations in neuronal mitochondrial trafficking for 3,4-methylenedioxymethamphetamine (MDMA; “ecstasy”) conjugated metabolites 5-(glutathion-S-yl)-N-methyl-α-methyldopamine [5-(GSH)-N-Me-α-MeDA] and 5-(N-acetylcystein-S-yl)-N-methyl-α- methyldopamine [5-(NAC)-N-Me-α-MeDA] are also provided.
Data Type
Conference Papers
Record ID
BIM-686063
American Psychological Association (APA)
Barbosa, Daniel Jose& Serrat, Roman& Ferreira, Luısa Maria& Branco, Paula Serio& Bastos, Maria de Lourdes& Capela, Joao Paulo…[et al.]. 2014-12-31. Neuronal mitochondrial trafficking impairment : the cause or a consequence of neuronal dysfunction caused by amphetamine-like drugs. International Meeting of Drug Abuse Research Society : Advances in the Neurobiological Basis of Inhalant Abuse (4th : 2013 : Mexico City, Mexico). . Vol. 3 (2014), pp.1-7.Cairo Egypt : Ashdin Publishing Corporation.
https://search.emarefa.net/detail/BIM-686063
Modern Language Association (MLA)
Barbosa, Daniel Jose…[et al.]. Neuronal mitochondrial trafficking impairment : the cause or a consequence of neuronal dysfunction caused by amphetamine-like drugs. . Cairo Egypt : Ashdin Publishing Corporation. 2014-12-31.
https://search.emarefa.net/detail/BIM-686063
American Medical Association (AMA)
Barbosa, Daniel Jose& Serrat, Roman& Ferreira, Luısa Maria& Branco, Paula Serio& Bastos, Maria de Lourdes& Capela, Joao Paulo…[et al.]. Neuronal mitochondrial trafficking impairment : the cause or a consequence of neuronal dysfunction caused by amphetamine-like drugs. . International Meeting of Drug Abuse Research Society : Advances in the Neurobiological Basis of Inhalant Abuse (4th : 2013 : Mexico City, Mexico).
https://search.emarefa.net/detail/BIM-686063
