Astrocyte responses to dopaminergic denervations by 6-hydroxydopamine and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine as evidenced by glial fibrillary acidic protein immunohistochemistry

Strömberg, Ingrid; Björklund, Håkan; Dahl, D.; Jonsson, Gösta; Sundström, Erik; Olson, Lar̀s

doi:10.1016/0361-9230(86)90119-x

Cited by 111 publications

(50 citation statements)

References 12 publications

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“…1, A and B); no further decrements in these measures were observed (data not shown). Chemically induced damage to the central nervous system, including damage caused by MPTP (19,23) causes reactive gliosis at the site of damage, the hallmark of which is an increase in GFAP. With our dosing regimen, MPTP caused a rapid induction of striatal GFAP mRNA (Fig.…”

Section: Stat3 Signaling and Astrogliosismentioning

confidence: 99%

“…Because MPTP can be administered systemically, it does not compromise the blood-brain barrier (19); therefore, blood-borne factors are unlikely to contribute to signaling events associated with gliosis (19,20). Antagonists of MPTPinduced dopaminergic neurotoxicity have been used to demonstrate that blocking neurotoxicity (21,22) completely blocks the induction of astrogliosis (19,23). Therefore, these drugs can be used to block signaling elements derived from the damaged targets to relate any observed changes to nerve terminal damaging effects, as opposed to potential pharmacological effects of MPTP.…”

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confidence: 99%

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Induction of gp130-related Cytokines and Activation of JAK2/STAT3 Pathway in Astrocytes Precedes Up-regulation of Glial Fibrillary Acidic Protein in the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Neurodegeneration

Sriram

Benkovic

Hebert

et al. 2004

Journal of Biological Chemistry

238

223

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Section: Stat3 Signaling and Astrogliosismentioning

confidence: 99%

mentioning

confidence: 99%

Induction of gp130-related Cytokines and Activation of JAK2/STAT3 Pathway in Astrocytes Precedes Up-regulation of Glial Fibrillary Acidic Protein in the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Neurodegeneration

Sriram

Benkovic

Hebert

et al. 2004

Journal of Biological Chemistry

238

223

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“…The dopamine-depleting 6-OHDA lesion of the median forebrain bundle has been shown to produce acute gliosis in the striatum as shown by increases in levels of the astrocyte marker GFAP. Stromberg et al demonstrated gliosis 1 month post-lesion which had down-regulated by 7 months post-lesion [28].In another study gliosis was at a peak in the first week postlesion but had declined to control levels after 4 months [27]. In studies where 6-OHDA was injected directly into the striatum there were increased numbers of astrocytes [28] and microglia [11] in the lesioned striatum.…”

Section: Discussionmentioning

confidence: 95%

“…Stromberg et al demonstrated gliosis 1 month post-lesion which had down-regulated by 7 months post-lesion [28].In another study gliosis was at a peak in the first week postlesion but had declined to control levels after 4 months [27]. In studies where 6-OHDA was injected directly into the striatum there were increased numbers of astrocytes [28] and microglia [11] in the lesioned striatum. In contrast, another study looking at GFAP levels in the striatum 15 months after a 6-OHDA lesion found no long-term gliosis [26].…”

Section: Discussionmentioning

confidence: 95%

In vivo transgene expression from an adenoviral vector is altered following a 6-OHDA lesion of the dopamine system

Torres

Monville

Löwenstein

et al. 2005

Molecular Brain Research

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We have investigated the in vivo dynamics of an adenovirus-based, LacZ expressing vector, RAd36, at different doses, when injected unilaterally into the corpus striatum of normal rats. We have further investigated the characteristics of this vector in the presence of a 6-OHDA lesion of the nigrostriatal pathway. The dopamine-depleting lesion had an effect on both the number and the distribution of cells transduced by the adenoviral vector. The lesioned side of the brain contained significantly greater numbers of β-galactosidase positive cells than the unlesioned side at 3 days, 1 week and 4 weeks post-injection and the distribution of transduced cells was altered by the presence of a dopamine lesion. We conclude that the increased levels of transgene expression seen in the lesioned hemisphere are due to a change in the diffusion characteristics of the injected vector in the lesioned hemisphere. These results indicate that, when investigating the use of virus-based vectors, ultimately for use in gene therapies in the CNS, the in vivo dynamics of the vector need to be assessed not only in the normal brain, but also in the pathological brain state such as animal models of target diseases.

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“…Historically, MFB lesion model is the most widely used [34,38,39]. Because the dopaminergic axons of the mesolimbocortical pathway also transverse the MFB, this meant that injecting MPTP at this site also lesioned the ventral tegmental cell bodies and their terminals in the forebrain.…”

Section: Discussionmentioning

confidence: 99%

Docosahexaenoic acid provides protective mechanism in bilaterally MPTP-lesioned rat model of Parkinson's disease

Hacioglu

Seval-Celik

Tanrıöver

et al. 2012

Folia Histochem Cytobiol.

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Docosahexaenoic acid (DHA), a major polyunsaturated fatty acid (PUFA) in the phospholipid fraction of the brain, is essential for normal cellular function. Neurodegenerative disorders such as Parkinson's disease (PD) often exhibit significant declines in PUFAs. The aim of this study was to observe the effects of DHA supplementation in an experimental rat model of PD created with '1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine' (MPTP). Adult male Wistar rats were divided into four groups: (1) Control; (2) DHA-treated; (3) MPTP-induced; and (4) MPTP-induced + DHA-treated. Motor activity was investigated using the 'vertical pole' and 'vertical wire' tests. The dopaminergic lesion was determined by immunohistochemical analysis for tyrosine hydroxylase (TH)-immunopositive cells in substantia nigra (SN). Immunoreactivities of Bcl-2, Akt and phosphorylated-Akt (p-Akt) in SN were evaluated by immunohistochemistry. MPTP-induced animals exhibited decreased locomotor activity, motor coordination and loss of equilibrium. Diminished Parkinsonism symptoms and decreased dopaminergic neuron death were detected in the MPTP-induced + DHA-treated group compared to the MPTP-induced group. Moderate decreases in Akt staining were found in the MPTP-induced and MPTP-induced + DHA-treated groups compared to controls. p-Akt immunoreactivity decreased dramatically in the MPTP-induced group compared to the control; however, it was increased in the MPTP-induced + DHA--treated group compared to the MPTP-induced group. The staining intensity for Bcl-2 decreased prominently in the MPTP-induced group compared to the control, while it was stronger in the MPTP-induced + DHA-treated group compared to the MPTP-induced group. In conclusion, DHA significantly protects dopaminergic neurons against cell death in an experimental PD model. Akt/p-Akt and Bcl-2 pathways are related to this protective effect

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Astrocyte responses to dopaminergic denervations by 6-hydroxydopamine and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine as evidenced by glial fibrillary acidic protein immunohistochemistry

Cited by 111 publications

References 12 publications

Induction of gp130-related Cytokines and Activation of JAK2/STAT3 Pathway in Astrocytes Precedes Up-regulation of Glial Fibrillary Acidic Protein in the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Neurodegeneration

Induction of gp130-related Cytokines and Activation of JAK2/STAT3 Pathway in Astrocytes Precedes Up-regulation of Glial Fibrillary Acidic Protein in the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Neurodegeneration

In vivo transgene expression from an adenoviral vector is altered following a 6-OHDA lesion of the dopamine system

Docosahexaenoic acid provides protective mechanism in bilaterally MPTP-lesioned rat model of Parkinson's disease

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