Methamphetamine-induced toxicity: An updated review on issues related to hyperthermia

Matsumoto, Rae R.; Seminerio, Michael J.; Turner, Ryan C.; Robson, Matthew J.; Nguyen, Linda; Miller, Diane B.; O’Callaghan, James P.

doi:10.1016/j.pharmthera.2014.05.001

Cited by 76 publications

(49 citation statements)

References 136 publications

(198 reference statements)

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“…Interestingly, a number of neuroprotective agents tested against METH toxicity were shown to lack significant effects on METH-induced hyperthermia (reviewed in Matsumoto et al, 2014). For example, that is the case for minocycline (Zhang et al, 2006), memantine (a NMDA antagonist) (Chipana et al 2008) or calcitriol (a vitamin D metabolite) (Cass et al, 2006) that proved to have neuroprotective effects in animals treated with METH without affecting METH-induced hyperthermia.…”

Section: Discussionmentioning

confidence: 99%

“…METH use can be lethal due to hyperthermia (Schep et al, 2010). In clinical emergency settings, elevations in body temperature are a common presenting symptom with few treatment options (Matsumoto et al, 2014). Additionally, METH addicts show several signs of neuropathology that include biochemical and structural abnormalities (Cadet et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Differential Effects of Environment-Induced Changes in Body Temperature on Modafinil’s Actions Against Methamphetamine-Induced Striatal Toxicity in Mice

et al. 2014

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Methamphetamine (METH) exposure can produce hyperthermia that might lead to toxicity and death. Modafinil is a wake-promoting compound that is also been prescribed off-label to treat METH dependence. Modafinil has shown neuroprotective properties against METH harmful effects in animal models. The goal of the present study was to test if the prevention of hyperthermia might play a role on the neuroprotective actions of modafinil against METH toxicity using various ambient temperatures. METH was administered to female C57BL/6 mice in a binge regimen: 4 × 5 mg/kg , 2h apart; modafinil (90mg/kg) was injected twice, 1h before first and fourth METH injections. Drugs were given at cold ambient temperature (14 °C) or hot ambient temperature (29 °C). Body temperature was measured during treatments. Brains were dissected out six days after treatments and processed for TH, DAT, GFAP and c-Fos immunohistochemistry. Exposure to hot ambient temperature exacerbated METH toxicity evidenced by sriatal reductions in TH and DAT and increased GFAP immmunoreactivity. Modafinil counteracted reductions in TH and DAT, but failed to block astroglial activation. At both ambient temperatures tested modafinil did induce increments in GFAP, but the magnitude was significantly lower than the one induced by METH. Both drugs induced increases in c-Fos positive nuclei; modafinil did not block this effect. Our results suggest that protective effects of modafinil against METH-induced neurotoxicity may be dependent, in part, to its hypothermic effects. Nevertheless, modafinil maintained some protective properties on METH-induced alterations in the striatum at different ambient temperatures.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Differential Effects of Environment-Induced Changes in Body Temperature on Modafinil’s Actions Against Methamphetamine-Induced Striatal Toxicity in Mice

et al. 2014

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“…While amphetamines are primarily associated with hyperthermia (Bowyer & Hanig, 2014;Matsumoto et al , 2014), acute decreases in body temperature are observed when they are administered at normothermic and lower ambient temperatures (Bowyer et al , 2001;Myles et al , 2008;Shortall et al , 2013) or at lower doses (Harkness et al , 2015), and particularly when animals are singly housed (Fantegrossi et al , 2008;Docherty & Green, 2010). Although MA-induced neurotoxicity is exacerbated by hyperthermia, (Bowyer et al , 1994;Miller & O’Callaghan, 2003;Sharma et al , 2015), neurotoxicity can still occur in its absence under the above conditions or when pharmacologically blocked (Albers & Sonsalla, 1995).…”

Section: Introductionmentioning

confidence: 99%

Trace amine-associated receptor 1 regulation of methamphetamine-induced neurotoxicity

et al. 2017

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Trace amine-associated receptor 1 (TAAR1) is activated by methamphetamine (MA) and modulates dopaminergic (DA) function. Although DA dysregulation is the hallmark of MA-induced neurotoxicity leading to behavioral and cognitive deficits, the intermediary role of TAAR1 has yet to be characterized. To investigate TAAR1 regulation of MA-induced neurotoxicity, Taar1 transgenic knock-out (KO) and wildtype (WT) mice were administered saline or a neurotoxic regimen of 4 i.p. injections, 2 hr apart, of MA (2.5, 5, or 10 mg/kg). Temperature data were recorded during the treatment day. Additionally, striatal tissue was collected 2 or 7 days following MA administration for analysis of DA, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and tyrosine hydroxylase (TH) levels, as well as glial fibrillary acidic protein (GFAP) expression. MA elicited an acute hypothermic drop in body temperature in Taar1-WT mice, but not in Taar1-KO mice. Two days following treatment, DA and TH levels were lower in Taar1-KO mice compared to Taar1-WT mice, regardless of treatment, and were dose-dependently decreased by MA. GFAP expression was significantly increased by all doses of MA at both time points and greater in Taar1-KO compared to Taar1-WT mice receiving MA 2.5 or 5 mg/kg. Seven days later, DA levels were decreased in a similar pattern: DA was significantly lower in Taar1-KO compared to Taar1-WT mice receiving MA 2.5 or 5 mg/kg. TH levels were uniformly decreased by MA, regardless of genotype. These results indicate that activation of TAAR1 potentiates MA-induced hypothermia and TAAR1 confers sustained neuroprotection dependent on its thermoregulatory effects.

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“…It was shown that METH increases the ROS production via various pathways [129, 130] including the inhibition of mitochondrial functions [131] and the stimulation of the NADPH oxidase (NOX) activity [132]. METH-induced ROS production is implicated in METH effects on neuronal degeneration [133, 134], toxicity in various cell types [135, 136], behavioral hyperactivity [137, 138], and hyperthermia [139, 140]. Notably, ROS-reducing agents including ROS scavengers and NOX inhibitors attenuate those effects of METH.…”

Section: Sig-1r-related Molecular Mechanisms and The Actions Of Cocaimentioning

confidence: 99%

Potential Molecular Mechanisms on the Role of the Sigma-1 Receptor in the Action of Cocaine and Methamphetamine

Yasui

2016

J Drug Alcohol Res

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The sigma-1 receptor (Sig-1R) is an endoplasmic reticulum membrane protein that involves a wide range of physiological functions. The Sig-1R has been shown to bind psychostimulants including cocaine and methamphetamine (METH) and thus has been implicated in the actions of those psychostimulants. For example, it has been demonstrated that the Sig-1R antagonists mitigate certain behavioral and cellular effects of psychostimulants including hyperactivity and neurotoxicity. Thus, the Sig-1R has become a potential therapeutic target of medication development against drug abuse that differs from traditional monoamine-related strategies. In this review, we will focus on the molecular mechanisms of the Sig-1R and discuss in such a manner with a hope to further understand or unveil unexplored relations between the Sig-1R and the actions of cocaine and METH, particularly in the context of cellular biological relevance.

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Methamphetamine-induced toxicity: An updated review on issues related to hyperthermia

Cited by 76 publications

References 136 publications

Differential Effects of Environment-Induced Changes in Body Temperature on Modafinil’s Actions Against Methamphetamine-Induced Striatal Toxicity in Mice

Differential Effects of Environment-Induced Changes in Body Temperature on Modafinil’s Actions Against Methamphetamine-Induced Striatal Toxicity in Mice

Trace amine-associated receptor 1 regulation of methamphetamine-induced neurotoxicity

Potential Molecular Mechanisms on the Role of the Sigma-1 Receptor in the Action of Cocaine and Methamphetamine

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