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Post intoxicative therapeutic immunization with myelin oligodendrocyte glycoproteine (MOG 35-55) suppresses spontaneous regeneration of dopaminergic neurons injured with 1-methyl-4 phenyl-1,2,3,6-tetrahydropiridine (MPTP)

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Balkowiec-Iskra E., Kurkowska-Jastrzebska I., Joniec I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 2
109-115
EN
The pathological process of neurodegeneration is accompanied by an inflammatory reaction that is believed to contribute to the pathogenesis of neurodegenerative diseases. The aim of our study was to evaluate the influence of autoimmune reaction induced by post-traumatic vaccination with myelin self-antigen on spontaneous regeneration of dopaminergic neurons, injured with MPTP. C57BL mice were intoxicated with 40 mg/kg MPTP and seven days later immunized with MOG 35-55 peptide in CFA. On 7th day following intoxication, the MPTP treated mice showed decrease of dopamine level by 63% as compared to the control mice. However, starting from the 14th day following intoxication, a spectacular increase of dopamine content was observed. Immunization with MOG resulted in statistically significant reduction of the increase in striatum as compared to non-immunized animals, and was lower by 23%, 17% and 15% on days 14, 28 and 50, respectively. Our results show suppressive influence of autoimmune reaction induced after injury on regeneration of dopamine cells intoxicated with MPTP.
2
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MHC class II positive microglia and lymphocytic infiltration are present in the substantia nigra and striatum in mouse model of Parkinson's disease

100%
Kurkowska-Jastrzebska I., Wronska A., Kohutnicka M., Czlonkowski A., Czlonkowska A.
Acta Neurobiologiae Experimentalis
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1999
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vol. 59
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issue 1
1-8
EN
We have studied MHC class II antigen expression and lymphocytic infiltration during dopaminergic neurone degeneration produced by intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridine (MPTP). Microglial activation was observed in the striatum and in the substantia nigra (SN) in this model. We noticed a marked increase of MHC class II antigen expression on microglia and T-cell recruitment in these regions after MPTP treatment. B-lymphocytes were not observed. T-cell infiltration predominantly consisted of CD8+ cells at every time point but CD4+ cells were present too. More than a half of the observed lymphocytes showed strong staining of CD44 antigen. Our findings suggest a possible immune system involvement in the pathological process following MPTP intoxication.
3
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Dopamine, serotonin and noradrenaline changes in the striatum of C57BL mice following myelin oligodendrocyte glycoprotein (MOG) 35-55 and complete Freund adjuvant (CFA) administration

86%
Balkowiec-Iskra E., Kurkowska-Jastrzebska I., Joniec I., Ciesielska A., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 4
379-388
EN
Many data suggest involvement of inflammation in neurodegeneration. However, the exact mechanisms of this cooperation are poorly understood. We have previously shown that induction of inflammatory reaction, both before and after injury of the striatum, affects regeneration of dopaminergic neurons. In the present research we studied the role of inflammatory reaction in non-injured striatum. We used myelin oligodendrocyte glycoprotein (MOG) 35-55 in complete Freund's adjuvant (CFA) to elicit experimental autoimmune encephalomyelitis (EAE) mice model. As determined by HPLC, striatal dopamine (DA) and serotonin levels in mice treated with either MOG 35-55 in CFA or CFA alone were significantly higher compared to vehicle-treated controls on 13th day after induction. The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Noradrenaline (NA) concentration did not differ between groups. Moreover, the striatal mRNA IL-1beta and TNF-alpha levels were elevated during induction phase of EAE in both groups, as determined by RT-PCR. Our data indicate regulatory connection between dopaminergic and immune systems.
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