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1

Memantine and memantine combined with HH or HBO decreases apoptosis and affects ex pression of Bcl-2, Bax and HIV 1A in brains of 7 days old rats in experimental hypoxiaschemia

100%
Gamdzyk M., Ziembowicz A., Salinska E.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Perinatal hypoxia ischemia (HI) is a frequent cause of neonatal brain injury. The aim of present study was to investigate the effect of combining HBO or HH with memantine on HI evoked apoptosis and on Bcl-2, Bax and HIF-1α expression in hippocampus and cerebral cortex of the brains of neonatal rats. METHODS: HI on 7-day old rats was induced by ligation of ipsilateral common carotid artery, followed by 75 min hypoxia. HBO (2.5 ATA) or HH (0.5ATA) were applied 1 or 6 h after H-I for 60 min. Memantine in dose of 20 mg/kg of body weight was applied 15 minutes before HBO or HH. These treatments were repeated for 3 following days. Expression of Bcl-2, Bax and HIF-1α was examined using western blotting. RESULTS: In our study we showed that memantine and combined therapies reduced number of apoptotic cells in brains of treated animals. Memantine applied 1 or 6 h after HI increased Bcl-2 expression in the ipsilateral hemispheres by, respectively, 41 and 9%. Memantine combined with HBO 1 or 6 h after HI upregulated Bcl-2 by 13 and 21%, respectively, and memantine combined with HH postconditioning upregulated it by 42 and 29%. The preliminary results show that both memantine alone and combined therapies changed Bax expression in ipsilateral brain hemisphere comparing to untreated HI. Our study showed also that memantine and memantine combined with HBO or HH affected expression of HIF-1α which controls several genes that play a key role in neuroprotective processes. CONCLUSIONS: Our results show that application of memantine alone and in combination with HBO or HH reduce apoptotic processes initiated by HI in developing brain. However, the neuroprotection achieved by combined therapies is not significantly bigger than that resulted from memantine alone. This project was funded by the National Science Centre based on decision nr DEC 2012/07/N/NZ4/02072.
2

Neuroprotective effects of metabotropic glutamate receptors group II (mGluR2/3) agonists in an animal model of brith asphyxia

100%
Bratek E., Ziembowicz A., Salinska E.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
Hypoxic-ischemic encephalopathy (HIE) results in permanent damage of the central nervous system that may result in neonatal death or developmental disorders. 20% – 30% of infants with HIE die in the neonatal period, and 33% – 50% of survivors demonstrate permanent neurodevelopmental abnormalities, such as cerebral palsy and mental retardation. It was shown recently that group II metabotropic glutamate receptor (mGluR2/3) activation before or after ischemic insult results in neuroprotection, but the exact mechanism of this effect is not clear. AIM(S): The aim of present study was to investigate whether mGluR2/3 activation after hypoxia‑ischemia reduces brain damage and if the reduction of the expression of pro-apoptotic factors is one of the mechanisms involved. METHOD(S): We used an animal model of hypoxia‑ischemia (H‑I) on 7‑day old rat pups. Animals were anesthetized and the left common carotid artery was isolated, double-ligated and then cut between the ligatures. After completion of the surgical procedure, the pups were subjected to hypoxia (7.4% oxygen in nitrogen for 75 min at 35˚C). Control pups were sham‑operated (anaesthetized and left c.c.a. dissected, but not ligated). Animals were injected intraperitoneally with specific mGluR2 (LY 379268) and mGluR3 (NAAG) agonists 1 h or 6 h after H‑I (5 mg/kg of body weight). The weight deficit of the ischemic brain hemisphere was measured and expression of Bax, Bcl‑2, and HTR/OMI was examined. Damage in the hippocampal CA1 region was examined by cresyl violet (CV) staining. RESULTS: Our results show that application of mGluR2/3 agonists after H‑I results in neuroprotection. Both applied agonists decreased brain tissue weight loss in ischemic hemisphere at both times of application (from 40% in H‑I to 15% – 20% in treated). Histological examination of the brain tissue showed that both mGluR2/3 agonists applied 1h or 6 h after H‑I decreased the damage of neuronal cells and the disorganization of CA1 region of hippocampus. Both agonist mGluR2/3 applied 1h or 6 h after H‑I were associated with decreased expression of BAX and HTR/OMI and increased expression of Bcl-2 in the ischemic brain hemisphere as compared to H‑I. CONCLUSIONS: The results show that activation of mGluR2 or mGluR3 in a short time after H-I insult triggered neuroprotective mechanisms and reduced apoptotic processes initiated by H‑I in the developing brain. FINANCIAL SUPPORT: This work was performed under the 2016/23/N/NZ7/01942 project.
3

Metabotropic glutamate receptors group II (mGLuR2/3) agonist exert neuroprotection by reducing apoptosis after hypoxic-ischemic preconditioning

100%
Bratek E., Ziembowicz A., Salinska E.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Perinatal asphyxia is characterized by clinical and laboratory evidence of acute brain injury due to asphyxia. It was shown that mGluR2/3 activation before or after ischemic insult results in neuroprotection but the exact mechanism of this effect is not clear. The aim of present study was to investigate whether mGluR2/3 activation after hypoxia-ischemia (HI) reduces brain damage and if the activation of antioxidant enzymes and decrease of oxidative stress. METHODS: We used an animal model of HI on 7-day old rat pups. Animals were anesthetized and the left common carotid artery was isolated and double-ligated and then cut between the ligatures. After completion of the surgical procedure the pups were subjected to hypoxia (7.4% oxygen in nitrogen for 75 min at 35°C). Animals were injected intraperitoneal with specific mGluR2 (LY379268) and mGluR3 (NAAG) agonists 24 h or 1 h after HI. First weight deficit of HI brain hemisphere were measured and examined the expression of Bax. Next in our investigation we were used TUNEL assay and TTC1% staining. RESULTS: Our results show a neuroprotective effect  of mGluR2/3 agonists.Both agonists applied decreased brain tissue weight loss in ischemic hemisphere independently on the time of application (from 40% in HI to 15–20% in treated). In our study we show the relative changes in the expression of Bax protein in ipsilateral and contralateral hemisphere. Our results show that both mGluR2/3 antagonists applied 24 h and 1 h after HI reduced number of TUNELpositive cells in ipsilateral hemispheres. We observed more number of TUNEL- positive cells in HI. Both mGluR2/3 agonists decreased area of ipsilateral hemisphere infraction. CONCLUSIONS: This study is the demonstration of the neuroprotective effect of mGluR2/3 agonist on neonatal HI brain injury. These data suggest the possibility that preconditioning reduces irreversible ischemic injury in part by decreasing apoptosis.
4

Hyperbaric treatment results in decreased ROS production in neonatal hypoxia-ischemia rat model

100%
Gamdzyk M., Ziembowicz A., Salinska E.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Encephalopathy caused by birth asphyxia results in significant mortality and long-term morbidity. In our previous studies we proved that HBO reduces brain damage in experimental model of birth asphyxia by almost 60%. The aim of present study was to evaluate the effect of hyperbaric oxygen (HBO) on reactive oxygen species (ROS) production and antioxidative enzymes activities – catalase (CAT) and glutathione peroxidase (Gpx) in 7-day old rat brain after hypoxia-ischemia (H-I). In the experimental model of H-I the left (ipsilateral) common carotid artery ligation is followed by 75 min hypoxia. HBO (2,5 ATA) was applied 1, 3 or 6 h after H-I for 60 min. Treatment was repeated for 3 following days. DCF test showed that H-I causes almost 4-fold increase in ROS production in ipsilateral hemisphere, while HBO reduced it by 40%, 24% and 18%, applied 1, 3 and 6 h after H-I, respectively. H-I resulted in 32% increase in catalase activity, probably as a compensation to high ROS concentration. HBO treatment reduced this increase to 4, 5 and 16%, respectively, which is probably a consequence of reduced oxygen radicals production. Similar pattern was observed in activity of Gpx. Our results suggest that HBO reduce synthesis of ROS (which manifests in decreased DCF fluorescence) and also decrease antioxidative enzymes activity. This may be one of the mechanism of HBO neuroprotective and diminishing brain injury effect.
5

TRPC3 and TRPV1 channels are engaged in memory consolidation in passive avoidance task in one-day old chicks

100%
Krolik A., Ziembowicz A., Salinka E.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: The stimulation of both ionotropic and metabotropic glutamate receptors and influx of calcium ions (Ca2+) into neurons is a crucial step in intracellular cascade of memory formation. Recently the existence of additional mechanism involved in intracellular Ca2+ increase, triggered by internal signals like increase of Ca2+ within the cell and activation of G protein coupled receptors, was demonstrated. This mechanism involves transient receptor potential (TRP) channels. AIM(S): The aim of our study was to investigate the participation of TRP channels in intracellular mechanisms engaged in memory consolidation METHOD(S): The model of passive avoidance task in one day old chicks was used. Chicks were injected with non-specific TRP channels antagonist SKF96365 or with specific antibodies against chosen TRP channels: TRPC3, TRPC5, TRPV1 and TRPV3. The injections were made into brain region connected with memory formation – intermediate medial mesopallium – immediately after training (time choice based on previous experiments) and animals were tested 2 h and 24 h after training RESULTS: The injection of SKF96365 and anti-TRPC3 antibody immediately after training resulted in strong task amnesia when tested 2 h and 24 h later. Injection of anti-TRPV1 and anti-TRPV3 antibody resulted in less manifested amnesia, whereas application of anti-TRPC5 antibody did not produce significant amnesia. CONCLUSIONS: Our results show that inhibition of TRPC3, TRPV1 and TRPV3 channels significantly disturbed memory of the task indicating on an involvement of these channels in memory formation. FINANCIAL SUPPORT: G1136-2014/15/B/NZ4/04487.
6

Hypobaric hypoxia and hyperbaric treatment prevents neuronal damage and affect antioxidative activity in neonatal hypoxia-ischemia rat model

100%
Gamdzyk M., Ziembowicz A., Salinska E.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Hypoxic–ischemic encephalopathy (HIE) remains a serious condition that causes significant mortality and long-term morbidity. The aim of the study was to evaluate the effect of hyperbaric oxygen (HBO), hyperbaric air (HBA) and hypobaric hypoxia (HH) on neonatal hypoxic–ischemic (HI) brain injury within a therapeutic window of 1–6 h. We used an experimental model of perinatal hypoxia–ischemia on 7-days old rats, where left (ipsilateral) common carotid artery ligation is followed by 75 min hypoxia. HBO, HBA (2.5 ATA) and HH (0.5 atm air) were applied at 1, 3 or 6 h after HI for 60 min. Treatment was repeated for 3 following days. Brain injury was assessed by comparing ipsilateral hemisphere and contralateral hemisphere weight. Based on the evaluation of weight ratio, HH, HBO and HBA treatment, regardless of time of treatment initiation, resulted in significant reduction of brain weight loss. We observed that HBO reduced brain damage by 58.1%, 57.6% and 54.9%, respectively to the time of treatment initiation (1, 3, 6 h after HI), HBA decreased the damage by 29.9%, 38.1% and 22.0% (respectively). HH also significantly lessened brain weight loss, from 38% after untreated hypoxia–ischemia to 12.9%, 23.1% and 23.8% after HH application respectively 1, 3 and 6 h after hypoxia–ischemia. Superoxide dismutase (SOD) activity and glutathione (GSH) concentration were also measured. HI caused decrease in GSH concentration and 6-fold increase in SOD activity in ipsilateral, but not contralateral hemisphere. HBO treatment applied 1 and 3 h after HI significantly increased GSH concentration and decreased SOD activity, the effect of HBA was less pronounced. HH treatment resulted in additional increase in SOD activity in both hemispheres. However, GSH concentration after HH returned to control values. HBO and HBA altered the expression of cytoplasmic SOD1, and these changes corresponded to changes in SOD activity, suggesting significant role of this protein in neuroprotecting properties of HBO. Our results suggest that HBO, HBA and HH may serve in attenuation of the effects of HI. Early treatment gives better results in brain protection. Our results suggest that HBO and HBA probably reduce synthesis of free oxygen radicals, which manifests in decreased SOD activity. HH however, seems to act on different mechanism, because it enhances SOD activity. It may be beneficial, as it helps to neutralize superoxide anion production, provided that this SOD activity increase is accompanied by activation of glutathione peroxidase (GPx) and catalase (CAT). This assumption needs further investigation.
7

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

100%
Duszczyk M., Ziembowicz A., Gadamski R., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
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.
8

Anti-apoptotic and pro-survival effect of group ii metabotropic glutamate receptors (MgluR2/3) activation in an animal model of birth asphyxia

100%
Salinska E., Ziembowicz A., Bratek E.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Birth asphyxia results in serious damage of central nervous system or neonatal death. It was shown recently that group II metabotropic glutamate receptors (mGluR2/3) activation results in neuroprotection but the exact mechanism of this effect is not clear. AIM(S): The aim of present study was to investigate whether neuroprotective effect of mGluR2/3 activation is connected with inhibition of apoptosis and activation of pro-survival neurotrophic factors. METHOD(S): We used hypoxia-ischemia (HI) on 7-day old rat pups as animal model of birth asphyxia. Animals were anesthetized and the left common carotid artery was isolated, double-ligated and cut between the ligatures. After 60 min of recovery the pups were subjected to hypoxia (7.4% oxygen in nitrogen for 75 min.). Control pups were sham-operated. Animals were injected i.p. with specific mGluR2 (LY379268) and mGluR3 (NAAG) agonists 1h or 6h after HI (5 mg/kg of b.w.). The weight deficit ofthe ischemic brain hemisphere was measured and the expression of Bax, Bcl-2, HTR/OMI was examined. The damage in the hippocampal CA1 region was examined by Cresyl violet staining. Differences in the expression of neurotrophic factors (BDNF, GDNF, TGF –beta) were measured using ELISA. RESULTS: Our results show that application of mGluR2/3 agonists after HI reduce brain damage. Both applied agonists decreased weight loss in ischemic hemisphere independently on the time of application by 50% and reduced the damage of CA1 region of hippocampus. Both mGluR2/3 agonists inhibited HI induced increase in expression of Bax and HTR/OMI and restored, decreased after HI, expression of Bcl-2. LY379268 and NAAG applied 1h or 6h after HI increased TGF beta expression and expression of BDNF and GDNF in the ischemic brain hemisphere. CONCLUSIONS: Neuroprotective effect of mGluR2/3 activation after HI insult is connected with reduction of apoptotic processes and activation of pro-survival neurotrophic factors. FINANCIAL SUPPORT: This work was made under MMRC-KNOW 2013–2017 project.
9

COX-2/PGI2 pathway is involved in neuroprotection induced by N1-methylnicotinamide in hypoxia/ischemia of newborn rats

100%
Slomka M., Ziembowicz A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
1-Methylnicotinamide (MNA) is a key metabolite of nicotinamide, which is an important cofactor in many metabolic pathways with intrinsic cytoprotective properties. Recent studies demonstrated that MNA induces in the periphery the anti-inflammatory and vasoprotective effects mediated by the COX-2/ PGI2 signaling pathway. The role of this pathway in the protection against ischemic injury has been emphasized by the increased risk of myocardial infarction, stroke or susceptibility to excitotoxic insults caused by COX-2 inhibitors. This suggests that administration of MNA resulting in activation of COX-2/PGI2 might provide neuroprotection in brain ischemia. The aim of this study was to evaluate neuroprotective abilities of MNA in the model of brain hypoxia/ischemia (HI) in 7-day old rat pups, and to assess its effects on COX-2 activity and eicosanoid levels in the ischemic brain. The results demonstrated that i.p. administration of 62.5 mg/kg MNA 30 min after HI induced a significant neuroprotection and a marked increase in COX-2 activity 6 and 24 h after the insult. This effect was not accompanied by changes in the COX-2 protein level, as measured with Western blotting. The analysis of the level of eicosanoids: 6-keto-PGF1alpha-a which is a stabile metabolite of PGI2, PGE2, and TXB2 in brain of rats treated with MNA after HI demonstrated in the ipsilateral cortex a significant increase in 6-keto-PGF1alpha 30 min after the treatment, while PGE2 and TXB2 levels did not change. Pretreatment with rofecoxib (COX-2 inhibitor) or indomethacin (unselective COX inhibitor) decreased the level of 6-keto-PGF1alpha in the ipsilateral cortex to values observed in the untreated ischemic brain. To test the hypothesis that neuroprotection evoked by MNA in HI model depends on activation of prostacylin receptors, the selective antagonist of these receptors RO 324479 was applied. However, pretreatment of rat pups subjected to HI with RO 324479 (10 mg/ kg i.p.) did not influence significantly the neuroprotective effect of MNA. Further studies are needed to assess the role of COX-2/PGI2 in the MNA-evoked neuroprotection.
10

Group I metabotropic giutamate receptors and ischemic preconditioning

100%
Duszczyk M., Gadomski R., Ziembowicz A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
11

Anxiolytic effects of mild hypobaric hypoxia in mice

100%
Duszczyk M., Ziembowicz A., Lzarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2009
|
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
12

Post-ischemic changes in NMDA-evoked CICR in synaptoneurosomes of the rat brain cortex and hippocampus

100%
Salinska E., Ziembowicz A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
13

NMDA-induced mitochondrial permeability transition in rabbit brain: in vivo and in vitro study

100%
Zieminska E., Matyja E., Ziembowicz A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
14

Analysis of putative toxic interaction of L-methylnicotinamide with dopaminergic neurons

100%
Slomka M., Ziembowicz A., Lazarewicz J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
It has been proposed that in the Parkinson’s disease exo- or endogenous N-methyl-compounds like 1-methylnicotinamide (MNA) could be accumulated by dopaminergic neurons and induces neurotoxic effects, as happens with MPP+. The aim of this study was to test this hypothesis by comparing direct effects of MPP+ or MNA application into the striatum of 7 day old rat pups and to the substantia nigra (SN) of the adult rats. Microinjections of tested substances in doses: MPP+ (20 and 100 μg) and MNA (20, 40, 80 μg), were made unilaterally. Effects of MNA and MPP+ on pups’ striatum were evaluated by TTC staining and the lesion volume was calculated using the ImageJ program. In the SN of adult rats alterations in the level of tyrosine hydroxylase (TH) immunostaining were examined at the 5th day after MPP+ or MNA injection, utilizing antibody specifi c to TH. Moreover the coronal sections (20 μm thick) of the SN were examined to evaluate MNA- or MPP+-induced glial activation with the glia-specifi c lectin. Using these methods we did not observe any toxic effect of MNA. MPP+ induced statistically signifi cant damages in the striatum of rat pups, whereas there was no lesion after MNA injection. Also in the SN of adult rats MPP+ caused 50% loss of TH-positive neurons and doubled the number of activated glial cells, while MNA injection had no visible effect. Summing up, present data did not demonstrate any toxic effects of MNA on dopaminergic neurons in the rat brain in vivo.
15

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

100%
Duszczyk M., Ziembowicz A., Gadamski R., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
16

Modulation of NMDA-evoked prostaglandin D2 release in rabbit hippocampus in vivo

88%
Lazarewicz J. W., Salinska E., Stafiej A., Ziembowicz A., Zieminska E.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
17

NMDA receptors and nitric oxide regulate prostaglandin D2 synthesis in the rabbit hippocampus in vivo

88%
Lazarewicz J. W., Salinska E., Stafiej A., Ziembowicz A., Zieminska E.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 4
The aim of this in vivo microdialysis study was to characterise the regulation of prostaglandin D2 (PgD2) synthesis by NMDA receptors in the rabbit hippocampus in relation to changes in extracellular Ca concentration ([Ca ]e) and nitric oxide (NO) levels. Samples of dialysate were analysed for changes in PgD2 concentration, in [Ca ]e and in the level of NO. The results demonstrated that a 20-min pulse application of 0.1 - 2.5 mM NMDA via a microdialysis probe induced a prolonged stimulation of PgD2 release that was sensitive to competitive NMDA receptor antagonists. An inhibitor of voltage-sensitive Na+ channels, tetrodotoxin, did not influence this effect but significantly suppressed basal PgD2 production, whereas a NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), prevented NMDA-evoked NO release and inhibited NMDA-induced PgD2 release in an L-arginine-sensitive manner. NO donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside, stimulated PgD2 release. NMDA-evoked decrease in [Ca2+]e was insensitive to TTX and L-NAME. These results demonstrate an in vivo NMDA receptor-mediated modulation of PgD2 synthesis in the brain, in which NO participates.
18

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

76%
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.
19

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

76%
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.
20

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

76%
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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