Methamphetamine (METH) causes reactive gliosis in vitro: Attenuation by the ADP-ribosylation (ADPR) inhibitor, benzamide

Sheng, Peilin; Cerruti, Catherine; Cadet, Jean Lud

doi:10.1016/0024-3205(94)00887-6

Cited by 22 publications

(15 citation statements)

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“…These temporal kinetics are similar to what other groups using binge dosing paradigms have reported (O'Callaghan and Miller, 1994; LaVoie et al, 2004; Thomas et al, 2004b). Although MA-induced glial activation is a well-established phenomenon in vitro , in rodents, and in humans (Sheng et al, 1994; Lau et al, 2000; Thomas et al, 2004a; Sekine et al, 2008; Yue et al, 2012; Clark et al, 2013), its role in MA-induced neurotoxicity is uncertain. Microglial activation precedes MA-induced dopaminergic terminal damage by one day in rats, suggesting that microglial activation could contribute to neural damage, rather than responding to it (LaVoie et al, 2004); and inhibiting microglial activation with MK-801 or dextromethorphan attenuates MA-induced DA depletion, though these agents also prevent hyperthermia, which may account for their neuroprotective effect (Thomas and Kuhn, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Neuroinflammation has been linked with several neurological disorders, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, and stroke (Czlonkowska and Kurkowska-Jastrzebska, 2011). It is well established that MA exposure activates microglia and astrocytes in culture as well as in animal and human studies (Sheng et al, 1994; Sekine et al, 2008; Krasnova and Cadet, 2009; Yue et al, 2012; Clark et al, 2013). Such gliosis may contribute to MA-induced neurotoxicity, as activated microglia and astrocytes produce reactive oxygen species that are harmful to neurons, and proinflammatory cytokines to propagate the neuroinflammatory cascade and recruit additional immune cells from the periphery, potentially amplifying the oxidative damage to neurons (Clark et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Characterization of binge-dosed methamphetamine-induced neurotoxicity and neuroinflammation

et al. 2015

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Methamphetamine (MA) is a potent, highly addictive psychostimulant abused by millions of people worldwide. MA induces neurotoxicity, damaging striatal dopaminergic terminals, and neuroinflammation, with striatal glial activation leading to pro-inflammatory cytokine and reactive oxygen species production. It is unclear whether MA-induced neuroinflammation contributes to MA-induced neurotoxicity. In the current study, we examined the linkage between the time course and dose response of MA-induced neurotoxicity and neuroinflammation. Adult male mice underwent a binge dosing regimen of four injections given every two hours with doses of 2, 4, 6, or 8 mg/kg MA per injection, and were sacrificed after 1, 3, 7, or 14 days. Binge MA treatment dose-dependently caused hyperthermia and induced hypoactivity after one day, though activity returned to control levels within one week. Striatal dopamine (DA) was diminished one day after treatment with at least 4 mg/kg MA, while DA turnover rates peaked after seven days. Although striatal tyrosine hydroxylase and DA transporter levels were also decreased one day after treatment with at least 4 mg/kg MA, they trended toward recovery by day 14. All doses of MA activated striatal glia within one day. While astrocyte activation persisted, microglial activation was attenuated over the two weeks of the study. These findings help clarify the relationship between MA-induced neuroinflammation and neurotoxicity, particularly regarding their temporal and dose-specific dynamics.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Characterization of binge-dosed methamphetamine-induced neurotoxicity and neuroinflammation

et al. 2015

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“…Anatomical evidence supporting the neurotoxic potential of METH stems from studies showing that a high dose of METH given to rats caused degeneration of dopamine (DA) nerve terminals, and loss of tyrosine hydroxylase (TH), DA transporter (DAT), tryptophan hydroxylase (TPH), and 5-hydroxytryptamine (5-HT) axon terminals (Axt and Molliver, 1991;Gibb et al, 1990;Ricaurte et al, 1982;Seiden and Sabol, 1996). Further support for the neurotoxic potential of METH comes from evidence that (a) high doses of METH cause striatal gliosis as shown by an increase of glial fibrillary acidic protein (GFAP) in rats and mice (Battaglia et al, 2002;O'Callaghan and Miller, 1994;Sheng et al, 1994), and (b) apoptotic pathways are involved in METH-induced neuronal injury .…”

Section: Introductionmentioning

confidence: 99%

Impairment in Consolidation of Learned Place Preference Following Dopaminergic Neurotoxicity in Mice is Ameliorated by N-acetylcysteine but not D1 and D2 Dopamine Receptor Agonists

Achat-Mendes

Anderson

Itzhak

2006

Neuropsychopharmacol

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Some of the major concerns related to methamphetamine (METH) abuse are the neuronal damage inflicted at dopamine (DA) nerve terminals and the cognitive deficits observed in human METH abusers. We have shown that a high dose of METH selectively depleted dopaminergic markers in striatum, frontal cortex and amygdala of Swiss Webster mice, and impaired learned place preference. In this study, we investigated whether deficits in consolidation of place learning, as a consequence of METH neurotoxicity, underlie the underperformance of cocaine conditioned place preference (CPP). Administration of METH (5 mg/kg Â 3) to Swiss Webster mice decreased striatal tyrosine hydroxylase (TH) immunoreactive neurons and significantly increased glial fibrillary acidic protein (GFAP) expression, confirming the neurotoxic potential of METH in mice. This treatment significantly attenuated the establishment of cocaine (15 mg/kg) CPP compared to control. To investigate whether manipulation of the consolidation phase improves learned place preference, mice were trained by cocaine and received daily post-training injections of DA receptor agonists or N-acetylcysteine (NAC). As memory consolidation occurs shortly after training, drugs were administered either immediately or 2 h post-training. Immediate posttraining administration of the D1 DA receptor agonist SKF38393 (5, 10, and 20 mg/kg) or the D2 DA receptor agonist quinpirole (0.25, 0.5, and 1.0 mg/kg) did not improve the establishment of CPP following METH neurotoxicity. However, immediate but not delayed NAC administration (50 and 100 mg/kg) enhanced cocaine CPP following METH neurotoxicity and had no effect on control CPP. The levels of the reduced form of glutathione (GSH) in striatum, amygdala, hippocampus and frontal cortex were significantly lower in METH-treated mice compared to control during the period of CPP training. Acute and repeated administration of NAC to METH-treated mice restored the decreased brain GSH but had no effect on controls. Results suggest that METH-induced dopaminergic neurotoxicity is associated with impairment of consolidation of learned place preference, and that this impairment is improved by immediate posttraining administration of the glutathione precursor NAC and not by D1 or D2 DA receptor agonists. Restoration of brain glutathione levels immediately post-training may facilitate the consolidation process.

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“…The latter finding was interpreted as evidence of gliosis, which would be consistent with elevated cerebral glucose metabolism (Roh et al 1998). Notably, exposure of rodents to MA induces gliosis in brain (Escubedo et al 1998; Sheng et al 1994). Increased cortical glucose metabolism during the first month of abstinence from MA, therefore, suggests that gliosis arises and/or increases during this period (Berman et al 2007).…”

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confidence: 99%

White-matter abnormalities in brain during early abstinence from methamphetamine abuse

et al. 2010

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BackgroundPrevious studies revealed microstructural abnormalities in prefrontal white matter and corpus callosum of long-term abstinent chronic methamphetamine abusers. In view of the importance of the early abstinence period in treatment retention, we compared 23 methamphetamine-dependent subjects abstinent from methamphetamine for 7–13 days with 18 healthy comparison subjects. As certain metabolic changes in the brain first manifest after early abstinence from methamphetamine, it is also possible that microstructural white-matter abnormalities are not yet present during early abstinence.MethodsUsing diffusion tensor imaging at 1.5 T, fractional anisotropy (FA) was measured in prefrontal white matter at four inferior–superior levels parallel to the anterior commissure–posterior commissure (AC–PC) plane. We also sampled FA in the corpus callosum at the midline and at eight bilateral, fiber-tract sites in other regions implicated in effects of methamphetamine.ResultsThe methamphetamine group exhibited lower FA in right prefrontal white matter above the AC–PC plane (11.9% lower; p = 0.007), in midline genu corpus callosum (3.9%; p = 0.019), in left and right midcaudal superior corona radiata (11.0% in both hemispheres, p’s = 0.020 and 0.016, respectively), and in right perforant fibers (7.3%; p = 0.025). FA in left midcaudal superior corona radiata was correlated with depressive and generalized psychiatric symptoms within the methamphetamine group.ConclusionsThe findings support the idea that methamphetamine abuse produces microstructural abnormalities in white matter underlying and interconnecting prefrontal cortices and hippocampal formation. These effects are already present during the first weeks of abstinence from methamphetamine and are linked to psychiatric symptoms assessed during this period.

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Methamphetamine (METH) causes reactive gliosis in vitro: Attenuation by the ADP-ribosylation (ADPR) inhibitor, benzamide

Cited by 22 publications

References 12 publications

Characterization of binge-dosed methamphetamine-induced neurotoxicity and neuroinflammation

Characterization of binge-dosed methamphetamine-induced neurotoxicity and neuroinflammation

Impairment in Consolidation of Learned Place Preference Following Dopaminergic Neurotoxicity in Mice is Ameliorated by N-acetylcysteine but not D1 and D2 Dopamine Receptor Agonists

White-matter abnormalities in brain during early abstinence from methamphetamine abuse

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