Inhibitors of Mitochondrial Respiration, Iron (II), and Hydroxyl Radical Evoke Release and Extracellular Hydrolysis of Glutathione in Rat Striatum and Substantia Nigra

Han, Jilin; Cheng, Fu‐Chou; Yang, Zhifei; Dryhurst, Glenn

doi:10.1046/j.1471-4159.1999.731683.x

Cited by 75 publications

(64 citation statements)

References 79 publications

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“…It is likely that GSH and glutathione peroxidase are elevated shortly after METH administration in response to defensive mechanisms against oxidative stress, but GSH is subsequently depleted. For instance, immediately following in vivo administration of the dopaminergic neurotoxin MPTP to rats a massive increase (5000%) of striatal GSH was observed (Han et al, 1999). However, it is well known that in Parkinson's disease there is reduction (40-50%) of GSH in substantia nigra and putamen (Dringen, 2000;Mandel et al, 2003).…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…Both directly (through catecholamine-and quinone-derived reactive oxygen species) and indirectly (through the formation of peroxynitrite), reactive oxygen species have been hypothesized to play a role in the sequelae of Parkinson's disease and its treatment with L-DOPA (Merad-Boudia et al, 1998;Spencer et al, 1998;Bonnet & Houeto, 1999;Han et al, 1999;Martinez et al, 1999; …”

Section: Discussionmentioning

confidence: 99%

The intracellular domain of p75NTR as a determinant of cellular reducing potential and response to oxidant stress

et al. 2005

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SummaryThe low-affinity neurotrophin receptor, p75NTR, has been found to be pro-or anti-apoptotic depending upon the cell in which it is expressed. Reactive oxygen species play a major role in apoptosis induction and enactment. Using two polyclonal PC12 populations that, respectively, do or do not express p75NTR, this paper demonstrates that p75NTR expression confers resistance to oxidant stress upon PC12 cells maintained in serum-containing medium. The effect of p75NTR on cell survival is mimicked in p75-negative cells by expression of constructs that produce the p75NTR intracellular domain (ICD) or p75NTR with the extracellular domain deleted (∆ ∆ ∆ ∆ ECD), suggesting that binding of an extracellular ligand to p75NTR is not required. Our studies further document that the differential sensitivity to oxidant stress is serum-dependent and associated with differential oxidation of glutathione between p75-positive and p75-negative cells. These results suggest that the role of p75NTR in determining the consequences and treatment of age-related disorders and conditions in which reactive oxygen species are involved may require neither the extracellular receptor domain nor, by inference, the cognate extracellular ligands of this neurotrophin receptor.

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“…The above reactions outline the potential role for iron in the pathophysiological cascade of the MPTP-induced neuronal death (56). In reality, misregulation of the iron metabolism and iron-induced oxidative stress are widely believed to be an important pathogenetic mechanism of neuronal death in PD (for review, see Ref.…”

Section: Discussionmentioning

confidence: 99%

“…The role of these GSH changes in the pathophysiological cascade of the MPTP-induced neuronal death has yet to be elucidated. GSH depletion by means of buthionine sulfoximine reportedly potentiates MPTP/MPP ϩ toxicity to nigral neurons (69,70); in addition, MPTP is known to induce an early increase in vivo in the release of glial GSH, which undergoes hydrolysis in the extracellular compartment (56). This mechanism might account in part for the early MPTP-induced decrease in GSH levels.…”

Section: Discussionmentioning

confidence: 99%

The Neurotoxin 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Induces Apoptosis in Mouse Nigrostriatal Glia

Serra

Sciola

Delogu

et al. 2002

Journal of Biological Chemistry

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Swiss mice were given 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 25 mg/kg/day, for 5 consecutive days and killed at different days after MPTP discontinuance. Decreases in striatal tyrosine hydroxylase activity and levels of dopamine and its metabolites were observed 1 day after MPTP discontinuance. Ascorbic acid and glutamate levels had increased, dehydroascorbic acid and GSH decreased, whereas catabolites of highenergy phosphates (inosine, hypoxanthine, xanthine, and uric acid) were unchanged. In addition, gliosis was observed in both striatum and substantia nigra compacta (SNc). Sections of SNc showed some terminal deoxynucleotidyl transferase-mediated 2-deoxyuridine 5-triphosphate nick end labeling (TUNEL)-positive cells. Neurochemical parameters of dopaminergic activity showed a trend toward recovery 3 days after MPTP discontinuance. At this time point, TUNEL-positive cells were detected in SNc; some of them showed nuclei with neuronal morphology. A late (days 6 -11) increase in striatal dopamine oxidative metabolism, ascorbic acid oxidative status, and catabolites of high-energy phosphates were observed concomitant with nigral neuron and nigrostriatal glial cell apoptotic death, as revealed by TUNEL, acridine orange, and Hoechst staining, and transmission electron microscopy. These data suggest that MPTP-induced activation/apoptotic death of glial cells plays a key role in the sequential linkage of neurochemical and cellular events leading to dopaminergic nigral neuron apoptotic death. Parkinson's disease (PD)1 is characterized by a selective loss of neurons in the substantia nigra compacta (SNc) and significant diminution of neostriatal content of dopamine and its major acidic metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). Consequently, the functioning of the nigrostriatal dopaminergic system is impaired. Although cellular and molecular pathways leading to neuronal death in PD are still unknown, major biochemical processes such as oxidative stress and impaired energy metabolism are involved (for review, see Ref.

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Inhibitors of Mitochondrial Respiration, Iron (II), and Hydroxyl Radical Evoke Release and Extracellular Hydrolysis of Glutathione in Rat Striatum and Substantia Nigra

Cited by 75 publications

References 79 publications

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

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

The intracellular domain of p75NTR as a determinant of cellular reducing potential and response to oxidant stress

The Neurotoxin 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Induces Apoptosis in Mouse Nigrostriatal Glia

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