Multiple methamphetamine injections induce marked increases in extracellular striatal dopamine which correlate with subsequent neurotoxicity
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Cited by (177)
The role of metabotropic glutamate receptors in neurobehavioral effects associated with methamphetamine use
2023, International Review of NeurobiologyCitation Excerpt :On the contrary, there is no FDA-approved pharmacotherapy for MUD. It is well established that acute neurobehavioral effects of meth are primarily mediated by the meth-induced reversal of monoamine transporter function and dramatic and prolonged rise in synaptic monoamine levels (Kogan, Nichols, & Gibb, 1976; O’Dell, Weihmuller, & Marshall, 1991; Robinson, Yew, Paulson, & Camp, 1990; Sulzer et al., 1995). Meth also increases monoamine levels via the inhibition/reversal of vesicular monoamine transporter-2 (VMAT2; Sulzer et al., 1995) and by blocking the activity of monoamine oxidases (MAOs).
Autophagy as a gateway for the effects of methamphetamine: From neurotransmitter release and synaptic plasticity to psychiatric and neurodegenerative disorders
2021, Progress in NeurobiologyCitation Excerpt :When administered chronically and/or at high doses, METH may produce toxicity in specific brain regions or even in peripheral organs, mostly those receiving dense sympathetic innervation (Albertson et al., 1999; Darke et al., 2008; Ferrucci et al., 2019; Matsumoto et al., 2014; Volkow et al., 2010a). Although METH neurotoxicity was initially considered to be relevant only for DA axon terminals, the occurrence of METH-induced toxicity has been documented at the level of neuronal cell bodies within the SNpc, and also the ventral tegmental area (VTA) (Ares-Santos et al., 2014; Biagioni et al., 2019; Fornai et al., 2003; Granado et al., 2010; Kitamura et al., 2007; Kitamura, 2009; Liu and Dluzen, 2006; Hirata and Cadet, 1997; Sonsalla et al., 1996; O’Dell et al., 1991; Wagner et al., 1980). To our experience, a certain amount of cell loss is detectable only when very high doses of METH are administered, which corresponds to a loss of nigrostriatal DA terminals ranging over 80 % (Biagioni et al., 2019; Fornai et al., 2003).
Thioredoxin-1 blocks methamphetamine-induced injury in brain through inhibiting endoplasmic reticulum and mitochondria-mediated apoptosis in mice
2020, NeuroToxicologyCitation Excerpt :Methamphetamine (METH) is a highly addictive stimulant drug whose illicit use and resultant addiction has become an alarming global phenomenon. Neurochemical studies have shown long-term neurotoxic effects of METH on monoamine and amino acid neurotransmitters including dopamine (O’Dell et al., 1991), glutamate (Stephans and Yamamoto, 1994), serotonin, and norepinephrine (Segal and Kuczenski, 1997) systems in several brain regions. METH enhances glutamate release in several brain regions, such as the ventral tegmental area (VTA) and nucleus accumbens (NAc) (Xue et al., 1996).
Evaluation the multi-organs toxicity of methamphetamine (METH) in rats
2020, Toxicologie Analytique et CliniqueCitation Excerpt :The study was done according to the Animal Ethics Committee Guidelines of Ilam University of Medical Sciences. In several studies conducted in the rat model, for the evaluation of long-term effects of METH on organs and tissues, doses of ≤ 5 mg/kg has been used [11,12]. So, in the present study 1, 2 and 4 mg/kg of METH were administered intraperitoneally as a solution in normal saline.
Effect of a binge-like dosing regimen of methamphetamine on dopamine levels and tyrosine hydroxylase expressing neurons in the rat brain
2019, Progress in Neuro-Psychopharmacology and Biological Psychiatry