Differential interactive effects of gliotoxin and MPTP in the substantia nigra and the locus coeruleus in BALB/c mice

Chang, Fang‐Chi; Wang, S.D.; Lu, Kuang Lieh; Lee, Eminy H.Y.

doi:10.1016/0361-9230(93)90215-w

Cited by 15 publications

(7 citation statements)

References 37 publications

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“…Also, while the present study focused on changes in the amygdaldpiriform area, a regional heterogeneity in sensitivity of astrocytes to OlAA is unlikely. This possibility has been rejected by Saffran and Crutcher (1987) and is not supported by our work in progress (M. Khurgel, unpublished observations), or by other studies (Chang et al, 1993;McBean, 1990;Takada and Hattori, 1986). We have used several astrocytic markers to monitor the viability of astrocytes following intracerebral injections of &.…”

Section: Discussioncontrasting

confidence: 49%

“…Already at 1 day p.i., swelling, accompanied by severe vacuolization and many membranous inclusions, was observed in soma and processes of astrocytes in the vicinity of the aAA injection (Takada and Hattori, 1986). Also, in a recent study Chang et al (1993) found that repeated injections of aAA result in a decrease in the amount of GFAP in substantia nigra and locus coeruleus. On the other hand, Saffran and Crutcher (1987) failed to obtain evidence in support of gliotoxic properties of aAA.…”

Section: Discussionmentioning

confidence: 95%

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Selective ablation of astrocytes by intracerebral injections of ?-aminoadipate

Khurgel

Koo

Ivy

1996

Glia

100

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Section: Discussioncontrasting

confidence: 49%

Section: Discussionmentioning

confidence: 95%

Selective ablation of astrocytes by intracerebral injections of ?-aminoadipate

Khurgel

Koo

Ivy

1996

Glia

100

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“…For instance, MPTP is converted to its toxic 1‐methyl‐4‐phenylpyridinium (MPP + ) metabolite by monoamine oxidase B (MAOB) in astrocytes [3, 4]. Evidence has shown that the specific gliotoxin α ‐aminoadipic acid or MAOB inhibitors can effectively block the toxicity of MPTP [5, 6]. By contrast, astrocytes treated with MPTP lose viability as a result of the generation of MPP + and the depletion of ATP induced by this toxic metabolite [7].…”

Section: Introductionmentioning

confidence: 99%

Effect of melatonin on temporal changes of reactive oxygen species and glutathione after MPP⁺ treatment in human astrocytoma U373MG cells

Chuang

Chen

2004

Journal of Pineal Research

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1-Methyl-4-phenylpyridinium (MPP(+)) ion, a toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, is produced by monoamine oxidase B in astrocytes. MPP(+) causes a selective dopaminergic neurodegeneration, the pathophysiologic hallmark of Parkinson disease. However, the toxic effect of MPP(+) on astrocytes remains unclear. Here, we examined the effect of MPP(+) on human astrocytoma U373MG cells, with particular attention to the temporal interaction of glutathione (GSH) and reactive oxygen species (ROS) (H2O2 and O). MPP(+) induced astrocyte apoptosis in a dose-dependent manner 48 hr after treatment. Distinctive early (<6 hr) and late (24-48 hr) responses were observed. ROS production and the oxidized GSH (GSSG)/GSH ratio, indicators of oxidative stress, rose dramatically after 24 hr of MPP(+) exposure, whereas the H2O2 level transiently decreased at 6 hr. ROS overproduction and GSH dysfunction were concomitantly associated with caspase-3 activation and finally led to cell apoptosis. Moreover, GSH depletion by diethyl maleate, but not buthionine sulfoximine, caused cells to die quickly and potentiated the cytotoxicity of MPP(+). Co-treatment with melatonin, a known antioxidant secreted by the pineal gland, significantly prevented cell apoptosis by inhibiting oxidative stress and caspase-3 activation, but it did not affect that the early changes due to MPP(+) treatment. Our results demonstrate that in astrocytes, GSH is involved in the early decrease and late increase in ROS levels induced by MPP(+) treatment. Melatonin remedies the dysfunction of GSH system to block caspase-3 activation and cell apoptosis induced by oxidative stress during the long-term exposure of MPP(+).

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“…Another possibility is that MPTP and CRF interact indirectly through other neurons. The PVN is known to receive noradrenergic (Leibowitz et al, 1988), adrenergic (Liposits et al, 1986), and serotonergic (Feldman et al, 1987) afferents other than the dopaminergic input (Liposits and Paull, 1989), and both norepinephrine and serotonin neurons were shown to be able to uptake MPTP and MPPf (Hu et al, 1991;Chang et al, 1993, Lee andLu, 1995). Moreover, these monoamine neurotransmitters were found in the amygdala (Fallon and Ciofi, 1992) and sim-ilar interactions could also occur in this area.…”

Section: Discussionmentioning

confidence: 99%

Alteration of corticotropin‐releasing factor immunoreactivity in MPTP‐treated rats

Huang

Lee

1995

J of Neuroscience Research

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A decrease of corticotropin-releasing factor (CRF) concentration has been reported in patients with Parkinson's disease (PD). The present study further examined the role of CRF in an animal model of parkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Results indicated that both subchronic (2 days) and chronic (7 days) MPTP treatments decreased the number of CRF immunoreactive neurons in both the paraventricular nucleus (PVN) of the hypothalamus and the central nuelcus of the amygdala (ACN). This effect lasted for almost a month after withdrawal of chronic MPTP injections. In addition, nomifensine pretreatment protected against MPTP's toxicity on DA neurons, as assessed by tyrosine hydroxylase immunoreactivity in the substantia nigra. However, the same treatment did not prevent the toxicity of MPTP on CRF neurons. Further, no significant difference was notable in the number of CRF immunoreactive neurons between normal young adult and normal middle-aged rats in both the PVN and the ACN. These results suggest that MPTP also produces a neurotoxicity on CRF neurons, and this effect is not secondary to MPTP's effect on DA neurons. Besides, altered CRF neuronal activity is involved in the process of pathological ageing, but not physiological ageing. Further, reduced CRF immunoreactivity in the PVN and ACN may imply alterations of neuroendocrine, autonomic as well as central functions caused by MPTP.

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Differential interactive effects of gliotoxin and MPTP in the substantia nigra and the locus coeruleus in BALB/c mice

Cited by 15 publications

References 37 publications

Selective ablation of astrocytes by intracerebral injections of ?-aminoadipate

Selective ablation of astrocytes by intracerebral injections of ?-aminoadipate

Effect of melatonin on temporal changes of reactive oxygen species and glutathione after MPP⁺ treatment in human astrocytoma U373MG cells

Alteration of corticotropin‐releasing factor immunoreactivity in MPTP‐treated rats

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Differential interactive effects of gliotoxin and MPTP in the substantia nigra and the locus coeruleus in BALB/c mice

Cited by 15 publications

References 37 publications

Selective ablation of astrocytes by intracerebral injections of ?-aminoadipate

Selective ablation of astrocytes by intracerebral injections of ?-aminoadipate

Effect of melatonin on temporal changes of reactive oxygen species and glutathione after MPP+ treatment in human astrocytoma U373MG cells

Alteration of corticotropin‐releasing factor immunoreactivity in MPTP‐treated rats

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Effect of melatonin on temporal changes of reactive oxygen species and glutathione after MPP⁺ treatment in human astrocytoma U373MG cells