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1

Protection of hippocampal neurons against neurotoxic damage by anti-myelin T cells may involve diminishing the activation of microglia and NG2+ glial cells

100%
Kurkowska-Jastrzebska L., Zaremba M., Oderfeld-Nowak R.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
We have previously demonstrated that CD4+ anti-myelin basic protein (MBP) T cells protect hippocampal neurons against trimethyltin-induced damage. In this study, we employ immunocytochemicalmethods to investigate the infl uence of administration of T cells to the response of microglia and of NG2+ cells to TMT-induced damage. Female Lewis rats were treated with anti-MBP CD4+ T cells (4 million per animal, i.v.) 24 hours after TMT (8 mg/kg, i.p.) intoxication. TMT caused degeneration of CA4 hipppocampal neurons and evoked an abundant reaction of microglial and NG2+ cells in the injured zone. The number of activated cells increased about 4-fold relative to controls as assessed on the 21st day after TMT treatment. A bulk of the cells of ameboid morphology, which expressed NG2 or microglial antigens, appeared in the zone of neurodegeneration. Interestingly, many of the cells of ameboid phenotype shared both antigens. Administration of T cells downregulated the activation of both glial classes and considerably reduced the formation of the ameboid phenotype forms. The latter were decreased, on average, by 60 percent. Our data suggest that the diminished activation of microglia and NG2+ cells, particularly the decrease of the ameboid forms known to release a number of proinfl ammatory substances, may contribute to the neuroprotective effect of T cells. Supported by the grant no N401-1293-33 of the Ministry of Scientifi c Research and Information Technology in Poland.
2

Inhibitory effects of 17beta-estradiol on production of both molecular and cellular factors in neuroinflammatory reaction in model of Parkinson's disease

64%
Ciesielska A., Joniec L., Cudna A., Kurkowska-Jastrzebska L., Sznejder A., Zaremba N., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
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2009
|
tom 69
|
nr 3
The neuroprotective action of 17β-estradiol (E2) against 1-methyl4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown in both female and male mice, however the exact mechanisms of that phenomenon remain obscured. We studied the chronic effects of E2 (0.25 mg per pellet, 21-days release) administered 7 days prior (Experiment 1) to or 3 days after (Experiment 2) MPTP intoxication (40 mg/kg, i.p.) in C57BL aged male mice on neurodegenerative and infl ammatory processes in nigrostriatal pathway. We estimated striatal: tyrosine hydroxylase (TH), glial fi brillary acidic protein (GFAP) content (Western blotting); cytokines (TNFα, TGFβ1, IFNγ), trophic factor (GDNF) gene expression (RT-PCR); CD4+ and CD8+ cells infl ux (immunohistochemistry) at 1, 7, 21 (Exp. 1) and 7, 21 (Exp. 2) days post intoxication. E2 exerted a neuroprotective effect upon nigrostriatal system when administered prior but also when administered after intoxication (E2 attenuated the MPTP-induced loss of TH). E2 also decreased the GFAP content. MPTP caused a rapid increase of TGFβ1, TNFα and IFNγ. Pre-treatment with E2 decreased the early expression of TGFβ1 and IFNγ but failed to suppress the MPTP-induced increase of TNFα. E2 pre-treatment also induced an increase of the GDNF and CD4+ cells infl ux to the injured brain areas but decreased the CD8+ cells infi ltration. The neuroprotective effects of E2 indicated in MPTP model might mediate through a modulation of neuroinfl ammatory reaction in lesioned nigrostriatal system.
3

Autoimmune encephalomyelitis is accompanied by the injury of hippocampal neurons

64%
Kurkowska-Jastrzebska L., Zaremba M., Cudna A., Piechal A., Swiatkiewicz M., Zaremba M., Czlonkowska A., Oderfeld-Nowak B.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Multiple sclerosis (MS) is associated with cognitive defi cits, developing independently from motor disorders. These defi cits may be associated with brain neuronal damage. In this study, using the experimental model for MS – autoimmune encephalomyelitis (EAE), we investigated whether EAE will result in the damage of hippocampal neurons and selective defi cits in learning and memory, and whether there may be a correlation between the two phenomena. Lewis rats 3 months old were injected with 4 millions of anti-MBP CD4+ T cells to evoke EAE. Animals suffered from tail and hind limb paresis and recovered after 10 dpi. T cells infi ltrated spinal cord and many brain regions including hippocampus. We demonstrated the decrease of pyramidal neurons in CA4 region by about 20%, as evaluated by stereological measurements, at 21 dpi. This was preceded by prolonged glial activation as well as by a rise of the pro-infl ammatory cytokine mRNA expression (IL-1β, IL-6 and TNF α). However, no differences in the water maze test were detected between the EAE and control groups, on 21 dpi and on 90 dpi. In conclusion, anti-MBP CD4+ T cells are capable of injuring hippocampal pyramidal neurons during EAE, probably, through the secretion of pro-infl ammatory cytokines. However, in the studied conditions, hippocampal neurodegeneration caused by T cells did not result in memory disturbances. Supported by the grant no N401- 1293-33 of the Ministry of Scientifi c Research and Information Technology in Poland.
4

The molecular and behavioral changes in the long-term observations in mice model of Parkinson's disease

64%
Zaremba M., Joniec L., Piechal A., Pyrzanowska J., Kurkowska-Jastrzebska L., Ciesielska A., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
The pathogenesis of non-motor symptoms in Parkinson’s disease (PD) is complex and not fully understood, but is believed to be related to the widespread nature of dopaminergic dysfunction involving structures beyond the substantia nigra. Therefore we’ve also focused in our experiments on specifi c brain regions (e.g. hippocampus and prefrontal cortex) critically involved in spatial learning and memory processes. One year old C57/BL male mice received 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine (MPTP) 40 mg/kg, and control group received 0.9 % NaCl. To evaluate spatial learning and memory abilities, the Morris water maze (WM) behavioral test was provided after 6 months from the intoxication. The brain concentration of monoamines: dopamine (DA), noradrenaline (NA), 5 – hydroxytryptamine (5-HT) and amino acid: glutamate (Glu) were determined by using high – performance liquid chromatography (HPLC). Statistical signifi cances differences in monoamines levels between groups were noticed in hippocampus (NA, DA content) and prefrontal cortex (NA content). We didn’t notice signifi cant differences in the WM test parameters between MPTP and the control animals. Correlation between the results of the behavioral testing in the probe trial and the level of monoamines were calculated. Swim distance to reach the hidden platform was negatively correlated with NA level in the hippocampus (rp=−0.62, P<0.05). There is need for a further investigation to confi rm the role for NA in spatial memories.
5

Neuroprotective effects of AAV2-h1L-10 in mouse model of Parkinson's disease

64%
Joniec L., Ciesielska A., Gladka A., Cudna A., Zaremba M., Kurkowska-Jastrzebska L., Hadaczek P., Bankiewicz H., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Parkinson’s disease (PD) is a neurodegenerative disorder which is characterized by abnormal loss of nigrostriatal dopamine (DA) neurons, accompanied by DA defi ciency in the striatum. The pathomechanism by which DA neurons degenerate is still unknown, however, there is increasing evidence that is possible immunological mechanisms involvement in the etiopathogenesis of PD. The aim of the present study was to examine the effect of an adeno-associated viral type-2 (AAV2) vector containing human interleukin-10 (hIL-10) gene on dopaminergic system restoration in the murine model of PD induced by by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Male C57BL/6 mice 12 months-old were used in this study. MPTP was injected in four intraperitoneal injections at 1-h intervals. AAV2-hIL-10 vector was bilaterally administered into striatum at 14, 21 or 28 days prior to MPTP intoxication. Animals were sacrifi ced at 7 days following MPTP injection. Striatal DA, DOPAC, HVA concentrations were quantifi ed by HPLC method; tyrosine hydroxylase (TH) mRNA expression was measured by RT-PCR method. MPTP treatment dramatically decreased DA concentration, signifi cantly decreased TH mRNA gene expression. AAV2-hIL-10 exerted a neuroprotective effect upon dopaminergic system (lower decrease in DA concentration). Additionally, viral vector administration prevented depletion of TH mRNA expression induced by MPTP. Our data suggest that AAV2-hIL-10 may play a neuroprotective role in MPTP mouse model of PD.
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