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1

Największe zimowisko karlika malutkiego Pipistrellus pipistrellus (Schreber, 1774) w Polsce

100%
Wojtowicz B., Duszczyk M.
Nietoperze
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2001
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tom 02
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nr 1
2

Behavioral evaluation of ischemic damage to CA 1 hippocampal neurons: Effects preconditioning

81%
Duszczyk M., Ziembowicz A., Gadamski R., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2006
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tom 66
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nr 4
In Mongolian gerbils, global forebrain ischemia induces enhanced locomotor activity and the disruption of nest building immediately after the insult, followed by damage to hippocampal neurons developing 3 days later. Preconditioning by a brief episode of sublethal ischemia induces the protection of CA1 hippocampal neurons against a lethal ischemic insult. We examined how preconditioning with 2-min ischemia affects disturbances in the nest building behavior and locomotor activity induced by the injurious 3-min ischemia. Morphological examination confirmed that preconditioning significantly reduced neuronal damage in CA1 evoked by injurious ischemia. Behavioral studies demonstrated that preconditioning reduced the locomotor hyperactivity and latency in nest building after test ischemia, in comparison to sham or naive animals. The results indicate that the nest building test and measurement of locomotor activity may be used for an early in vivo prediction of the extent of ischemic brain damage and tolerance induced by ischemic preconditioning.
3

Vaccine preservative, thimerosal, affects pain sensivity, body temperature and prefrontal cortex in rats

81%
Duszczyk M., Olczak M., Mierzejewski P., Majewska M.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
Mercury compounds are known neurotoxins. Thimerosal (THIM), which contains molecularly 49% of mercury, is added as preservative to many child vaccines and is suspected to be a major factor in autism pathogenesis. Data from Adverse Event Reporting of the Center for Disease Control and Prevention (USA) provide epidemiological evidence for a link between mercury exposure from THIM-containing vaccines and autism or other neurodevelopmental disorders. Our earlier studies showed that neonatally administered THIM causes persistent changes in pain reactivity, which are manifested in adult rats. In this study we investigated acute effects of THIM on pain reactivity, body temperature and brain glutamatergic system in mature rats. Single injection of THIM induced marked hypoalgesia, measured in hot plate test. This effect was time- and dose-dependent. It was reversed by administration of naloxone before the test and by two neurosteroids – dehydroepiandrosterone sulfate and androsterone. THIM also caused a dose-dependent hypothermia. Administration of THIM directly to the prefrontal cortex of freely moving rats increased the extracellular concentration of glutamate. The results suggest that acute THIM injection rapidly changes the neurochemical systems related to glutamate, opioid peptides, and probably GABA, which may contribute to developmental and neurotoxic effect of this compound. Funded by EC grant MEXC-CT-2006-42371 to M. D. Majewska.
4

Group I metabotropic giutamate receptors and ischemic preconditioning

81%
Duszczyk M., Gadomski R., Ziembowicz A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
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nr 3
5

Anxiolytic effects of mild hypobaric hypoxia in mice

81%
Duszczyk M., Ziembowicz A., Lzarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2009
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tom 69
|
nr 1
Mild hypobaric hypoxia (MHH) which is known to induce tolerance to brain hypoxia/ischemia, appeared to prevent development of anxiety and depressive-like behavior in rats submitted to the unavoidable adversive stress. The latter effect of unclear mechanism so far wasnít confi rmed in other animal models. Since enhanced brain expression of the neuropeptide Y (NPY) mimics effects of anxiolytic and antidepressant drugs, and we noticed that MHH increases the number of NPY-positive neurons in the gerbil hippocampus, we propose possible involvement of NPY in the positive behavioral effects of MHH. The aim of present study was to reproduce behavioral effects of MHH in balb/c57 mice using the tail suspension test and the elevated plus maze, and to evaluate immunohistochemically in these animals the number of NPY-positive neurons in the hippocampus. We confi rmed that intermittent MHH (360 Torr, 2 h for 3 consecutive days) in mice induces anxiolytic and weak antidepressant-like effects. The elevated plus maze trials performed 48 h after MHH revealed a signifi cant increase in frequency of the open arm entries, reduced duration of the closed arm occupancy, and 7-fold increased time spent on the open arms in comparison to sham animals. In the tail suspension a signifi cant decrease of the duration of immobility was observed 24 h, but not 48 h after MHH, when we detected a modest but signifi cant increase in the number of NPY-positive neurons in the hippocampus. Thus, although our preliminary data confi rm anxiolytic and antidepressant-like effects of MHH in mice, further studies are needed to characterize better these effects and to learn its mechanism, particularly to verify the role of NPY. Supported by the Scientifi c Network Fund no 26/E-40/SN0023/2007
6

Early postnatal thimerosal administration, in a vaccination-like scheme, causes vast structural damage in rat brain: implication for autism

81%
Olczak M., Duszczyk M., Mierzejewski P., Majewska M.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Thimerosal (THIM), an organomercury compound added to many child vaccines, is a prime suspect as agent causing autism epidemic. Data analysis from Vaccine Adverse Event Reporting System (CDC,USA) revealed that children immunized with THIM containing vaccines are several times more likely to develop autism and other neurodevelopmental disorders than those, who received THIM-free vaccines. In this study we examined developmental neurotoxic effects of THIM administered to Lewis and Wistar rats i.m. in four equal doses (12 μg Hg/kg to 3 mg Hg/kg) on postnatal days 7–14. Analysis of Hg content in brains of THIM-treated animals showed signifi cant amounts of Hg, which remained there for longer than 30 days. When animals reached maturity their brains were removed and examined for histopathological changes using H&E and immunohistochemistry staining (GFAP, synaptophysin, neurofi laments, dopamine, opiate receptors). Vast structural damage was found in the brains of THIM-treated animals: reduced number of Purkinie cells, ischemic and necrotic changes in the amygdala, ischemic and cell structure abnormalities in the temporal neocortex, dorsal and ventral hippocampus; hippocampal, pontal and cerebellar clasmatodendrosis, loss of synaptic junctions in hippocampus. These neuropathological changes correspond with behavioral alterations observed in THIM-treated rats and seem analogous to structural brain abnormalities found in autistic patients. Funded by EC grant MEXC-CT-2006-42371 to M.D. Majewska.
7

Behavioral evaluation of ischemic damage of CA1 hippocampal neurons:effects of preconditioning

81%
Duszczyk M., Ziembowicz A., Gadamski R., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
8

NMDA receptor antagonists - a novel approach at the phenomenon of neuroprotection

71%
Makarewicz D., Duszczyk M., Kuszczyk M., Lazarkiewicz J., Salinska E.
Acta Neurobiologiae Experimentalis
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2011
|
tom 71
|
nr S
Alternative methods of the therapy in the brain ischemia such as preconditioning seem more interesting because of the lack of the clinical applicable effective pharmacological neuroprotection. The role of NMDA receptor activation in triggering of this phenomenon was suggested, but it is not clear. Our recent in vitro studies (Kuszczyk et al. 2010) disclosed tolerance to the excitotoxic challenge by preconditioning with different NMDA receptor antagonists including MK-801 and memantine. The aim of the present study was to check if NMDA receptor antagonism induces also brain tolerance in vivo in different models of experimental brain ischemia. They included hypoxia-ischemia (H-I) in 7-dayold rats and 3-min global forebrain ischemia of Mongolian gerbils. In the neonatal rats exposure to 7% O2 in N2 was used for hypoxic preconditioning (H-P) as a positive control, while for pharmacological preconditioning two NMDA receptor antagonists MK-801 (3 mg/kg) and memantine (5 mg/kg) were injected i.p. Gerbils were pretreated with MK-801. The animals were preconditioned 24, 48, 72 and 96 hours before the insults, and the brain damage or deficit of CA1 pyramidal neurons was evaluated two weeks later. Our results demonstrated that MK-801 administered in all studied time points almost completely reduced brain damage compared to the H-I group, while H-P and preconditioning with memantine were less effective. In gerbils MK-801 was effective only 24 h before global ischemia. These data demonstrate for the first time ischemic tolerance induced by MK-801 and memantine preconditioning in vivo. Known neuroprotective effects of the NMDA receptor antagonists in various models of brain ischemia may be partially ascribed to induced tolerance. We consider a role of mild oxidative stress and enhanced production of trophic factors in its mechanisms. Supported by the MNiSW grant #0664/B/ P01/2010/38.
9

Antidepressant-like and anxiolytic-like effects of mild hypobaric hypoxia in mice: possible involvement of neuropeptide Y

61%
Duszczyk M., Gamdzyk M., Ziembowicz A., Boguszewski P. M., Lazarewicz J. W., Salinska E.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr 4
Previous studies have demonstrated that repeated submission of rats to mild hypobaric hypoxia reduces the persistent behavioral and hormonal depressive symptoms induced by exposure to footshock in the learned helplessness paradigm. The aim of this study was to determine whether hypoxic preconditioning of mice can also induce antidepressant- and anxiolyticlike effects that are detectable with the other commonly used behavioral tests, and to determine whether these effects are accompanied by an increase in neuropeptide Y (NPY) in the hippocampus, which may suggest the involvement of NPY in these mechanisms. The intermittent mild hypobaric hypoxia was generated by 2-h exposure of mice to 0.47 atm for 3 consecutive days. In the tail suspension test a significant decrease in the duration of immobility was observed 24 h, but not 48 h after the last hypobaric session. The elevated plus maze trials performed 48 h after preconditioning showed a significant increase in the frequency of open arm entries, a reduction in the duration of closed arm occupancy and substantially more time spent in the open arms in comparison to the control groups. The open field test demonstrated the absence of increases in general activity or unspecific exploratory behavior in hypoxia-preconditioned mice. The EIA test detected a statistically significant but relatively weak increase in the NPY content in the hippocampus 24 h after preconditioning. Together, our data demonstrate that preconditioning of mice with intermittent mild hypobaric hypoxia induces anxiolytic- and antidepressantlike effects. They are accompanied by up-regulation of NPY which may suggest its mechanistic role.
10

Hyperbaric preconditioning combined with post-ischemic hyperbaric therapy prevents ischemia-evoked damage to CA1 hippocampal neurons of Mongolian gerbils

61%
Malek M., Gamdzyk M., Duszczyk M., Ziembowicz A., Sobczuk A., Lazarewicz J., Salinska E.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Lack of the clinically effective pharmacological neuroprotection in different forms of brain ischemia increased the interest in alternative methods of therapy, like hypothermia or induction of brain tolerance by pre- and post-conditioning. The hyperbaric oxygen (HBO) therapy (2.5 atm) applied after ischemia or traumatic brain injury is one of the proposed but still controversial methods. The aim of this study was to find whether HBO and hyperbaric air (HBA) preconditioning followed by hyperbaric treatment applied for 60 min at different times after 3 min forebrain ischemia in gerbils will give a significant protection. The effects of both treatments on brain temperature and animal behaviour were also examined. A telemetric system to measure brain temperature was used and for behavioural observations a nest building test. The density of viable CA1 pyramidal neurons was also quantified. Our results show that HBO preconditioning combined with HBO postischemic therapy significantly reduced ischemia-evoked increase of brain temperature. HBA was also effective. Both treatments significantly increased gerbils’ ability to build a nest in comparison to untreated animals. The best effect was observed when postischemic therapy was applied 1 h after ischemia, but it was also effective 3 h after ischemia. Morphological analysis showed that HBO preconditioning combined with HBO postischemic treatment applied 1 h after ischemia significantly reduced neuronal damage in CA1 region of hippocampus resulting in 85% of surviving neurons compared to 18% of surviving CA1 neurons in the brains of animals subjected to ischemia but not treated with HBO. Our results show that HBO preconditioning combined with HBO therapy after forebrain ischemia in gerbils gives morphological protection which is accompanied by good behavioral results. Apart from inducing tolerance mediated by mild oxidative stress, HBO may affect blood oxygenation and other factors instrumental in brain protection.
11

Neuroprotective potential of 1-methyl-1,2,3,4,-tetrahydroisochinoline in brain ischemia: role of NMDA receptor antagonism

61%
Duszczyk M., Kuszczyk M., Makarewicz D., Salinska E., Antkiewicz-Michaluk L., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Various endogenous teterahydroisochinoline derivatives present in the mammalian brain have been considered as neurotoxic substances. However 1-methyl-1,2,3,4-tetrahydroisochinoline (1MeTIQ) is known for its mild neuroprotective potential of the unclear mechanism. On the one hand 1MeTIQ exhibits anti-dopaminergic activity and reduces the neurotoxic effects of MPTP and rotenone, decreasing also the behavioral effects of MK-801 in rats in vivo. On the other hand the results of our previous study demonstrated that 1MeTIQ in vitro prevents glutamate-induced excitotoxicity in cultured neurons suggesting that this effect may be ascribed to its inhibitory effect on NMDA receptors. It is well known that the antagonists of NMDA receptors provide neuroprotection in brain ischemia, however the anti ischemic properties of 1MeTIQ were not tested previously. The aim of our present study was to verify in vitro putative antagonistic effects of 1MeTIQ on the NMDA receptors and to evaluate its neuroprotective potential in the animal models of brain ischemia. The receptor binding experiments using membranous fractions isolated from the rat brain cortex confirmed that 1MeTIQ in high micro molar concentrations inhibits in a concentration-dependent manner the specific binding of [3H] MK-801, while the binding of [3H]glutamate remains unaffected. The hypothesis that 1MeTIQ may be attributed to NMDA receptor antagonists acting as channel blockers was also supported by the results of experiments utilizing primary cultures of rat cerebellar granule cells submitted to acute NMDA and glutamate excitotoxicity. Under these conditions 1MeTIQ applied at high micro molar concentrations provided a pronounced neuroprotection and significantly inhibited generation of the calcium signal. The in vivo ischemic experiments demonstrated that application of 1MeTIQ in the dose of 50 mg/kg 30 min before the insult in the model of global forebrain ischemia in Mongolian gerbils or its repeated application in the same dose after hypoxia-ischemia in the rat model of perinatal asphyxia provided significant neuroprotection. In the gerbils treated with 1MeTIQ we observed the morphological and behavioral symptoms of neuroprotection and the postischemic hypothermia characteristic for medication of brain ischemia with the NMDA receptor antagonists. Collectively these data offer new arguments confirming the hypothesis that 1MeTIQ acts as a weak uncompetitive antagonist of NMDA receptors, providing the neuroprotection under various excitotoxic and ischemic conditions both in vitro and in vivo.
12

Neuroprotective potential of methylnicotinamide versus liicotinamide in vivo and in vitro

61%
Slomka M., Makarewicz D., Zieminska E., Duszczyk M., Stafiej A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
13

Differential efficacy of mild normobaric hypoxia in inducing ischemic tolerance in two models of brain ischemia in vivo

61%
Duszczyk M., Makarewicz D., Malek M., Ziembowicz A., Lazarewicz J., Salinska E.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Induction of short ischemic episodes after the stroke can be neuroprotective. Hypoxia was also suggested as the factor producing neuroprotection in the animal brain. Therefore in our studies we aimed to test if normobaric hypoxia (10% of oxygen) induced after ischemia could prevent neuronal loss. The model of hypoxia-ischemia (H-I) in 7-days old rats and the model of global forebrain ischemia in Mongolian gerbils were used. 7-days old rats were subjected to H-I and the first of three episodes of postconditioning hypoxia was induced 1, 3 or 6 hours after H-I episode. After ischemia gerbils were subjected to three trials of 1h hypoxia applied every 24 hours. The first episode was induced immediately, 2.5 h or 6 h after the ischemic insult. The morphological and behavioral effects of the postconditioning were evaluated. In the model of H-I on rats, the assessment of brain mass deficit revealed that normobaric hypoxia induced signifficant neuroprotection when applied 1 h or 6 h after H-I but not 2.5 h. In the global forebrain ischemia model normobaric hypoxia itself was harmless and the number of pyramidal neurons evaluated in CA1 region was the same as in the sham group. The neuroprotective effect of normobaric hypoxia postconditioning was observed when hypoxia was induced immediately after ischemia but not 2.5 or 6 hours after the insult. The behavioral evaluation showed only small improvement in nest-building test in postconditioned animals. Presented data show that normobaric hypoxia postconditioning produces the neuroprotective effect, however the therapeutic window of this treatment varies according to the model of brain ischemia. Supported by MSHE grant NN401003935.
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