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1

Characterization and modulation of calcium ionophores activated by NMDA and non-MNDA-receptor stimulation

100%
Salinska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
1992
|
tom 52
|
nr 3
2

Early and delayed hypoxic postconditioning in the model of birth asphyxia in 7-day-old rats

100%
Makarewicz D., Salinska E.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Lack of the clinically applicable effective pharmacological neuroprotection in different forms of brain ischemia triggers increasing interest in alternative methods of therapy, including induction of brain tolerance by pre- and postconditioning. It is known for a long time that hypoxic preconditioning reduces brain damage in the rat model of perinatal asphyxia (Vannucci et al., 1998, Cantagrel et al., 2003). Recent data demonstrate that also postconditioning with moderate hypoxia delayed for 24 h after the insult results in a modest brain neuroprotection in adult mice (Leconte et al., 2009), however similar studies using the immature rats were never done. It has been suggested that similar mechanisms are involved in the induction of tolerance to brain ischemia by pre- and postconditioning, but timing may differ in both cases. Two temporal profiles of brain tolerance induced by preconditioning have been recognized: an early tolerance induced within minutes and depending on fast posttranslational modifications of proteins and a delayed one, developing after several hours to days and dependent on de novo protein synthesis (Kirino, 2002). It is not clear whether brain tolerance to hypoxia/ischemia induced by hypoxic postconditioning is also a two-phase phenomenon. The aim of this study was to evaluate efficacy of normo- and hypobaric postconditionig initiated 1, 3, or 6 hours after the insult in 7-day-old rats submitted to hypoxia-ischemia (H-I). H-I was induced by ipsilateral carotid occlusion followed by 75 min. exposure to hypoxia (7.2 - 7.4% O2 in N2). Hypoxic postconditionig was conducted under normobaric conditions at 10% O2 in N2 for 75 min, or in the hypobaric chamber set at 360 torr corresponding to 10 % O2 at the sea level. The post-conditioning was repeated once a day for 3 consecutive days. The brain damage was evaluated two weeks after H-I and expressed as ipsilateral hemisphere weight deficit in percent of the contralateral hemisphere. The results of this study demonstrated that both, normobaric or hypobaric postconditioning resulted in a significant neuroprotection only if initiated 1 h or 6 h after H-I, but not after 3 h. These results demonstrate for the first time efficacy of hypoxic postconditioning in the rat model of H-I and suggest that depending on timing of the hypoxic postconditioning the early and delayed tolerance may be achieved. Experiments are in progress verifying the role of mild oxidative stress in the mechanism of hypoxic postconditioning. Supported by the Ministry of Science and Higher Education grant #0039/B/P01/2008/35.
3

Agonist-activated Ca2plus and Co2plus influx through divalent cation-permeable kainate receptors

100%
Salinska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
4

Role of calcium in glutamate-mediated toxicity ; mechanisms of calcium fluxes in rabbit hippocampus in vivo investigated with microdialysis

100%
Lazarewicz J. W., Salinska E.
Acta Neurobiologiae Experimentalis
|
1993
|
tom 53
|
nr 1
5

Modulation of NMDA receptor-mediated release of [3H]arachidonate in hippocampal slices of immature rats

100%
Salinska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 1
6

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

81%
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.
7

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

81%
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.
8

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

81%
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.
9

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

81%
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.
10

Inhibition of mGluR1 and mGluR5 impairs memory consolidation and reconsolidation by disregulation of local protein synthesis

81%
Slomka M., Lenart J., Salinska E.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
It is known that mGluRs group I (mGluR1 and mGluR5) are involved in memory consolidation and reconsolidation probably by local protein synthesis regulation. One of the consequences of group I mGluRs activation is the synthesis of new proteins that play important role in memory consolidation and reconsolidation – NCAM and CaMKII, and also FMRP, that plays an important role in the mRNA transport and regulation of mRNA translation in the nerve endings by a negative-feedback mechanism. The aim of this study was to investigate the effect of mGluR1 and mGluR5 inhibition on synthesis of NCAM, CaMKII and the regulatory protein FMRP. In our experiments the passive avoidance task in one-day chicks was used and mGluRs 1/5 were inhibited by intracerebral injection of specific inhibitors, LY367385 and MPEP respectively. The expression of chosen proteins was determined in nerve endings isolated from chick brain. Our results show, that inhibition of each receptor around the time of training resulted in decrease of NCAM and CaMKII synthesis, as well as in synthesis of FMRP. However, the inhibition of mGluR1/5 around the time of reminder resulted in increase in NCAM and CaMKII synthesis, although synthesis of FMRP was significantly decreased. These results suggest that both receptors are involved in memory formation by regulation of termination of protein synthesis through control of FMRP synthesis.
11

Tetrabromobisphenol A directly interferes with activity of NMDA isolated cortical membranes

81%
Diamandakis D., Zieminska E., Salinska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: The results of early studies suggested a role of glutamate receptors in the mechanism of increases in intracellular Ca2+ concentration ([Ca2+]i ) and cytotoxicity induced by the brominated flame retardant, tetrabromobisphenol-A (TBBPA). Although now interest has focused mainly on TBBPA-induced Ca2+ release from intracellular stores, here we revisited the former issue and tested the involvement of NMDA receptors (NMDARs) in Ca2+ imbalance in neurons induced by TBBPA. METHODS: These effects were examined in primary cultures of rat cerebellar granule cells (CGC), and then, using isolated cortical membranes we checked whether TBBPA directly interacts with the agonist and modulatory sites of the NMDAR complex. On the 7th day in vitro CGC were treated with TBBPA at low µM concentrations. 45Ca uptake was detected and changes in [Ca2+]i , and plasma membrane potential were measured using fluorescent probes fluo-3 and oxonol VI, respectively. Moreover effects of TBBPA on specific binding of [3 H]MK-801, [3 H]glutamate and [3 H]glycine to isolated fraction of the rat brain cortex membranes were studied. RESULTS: The results demonstrated that TBBPA concentrationdependently increased 45Ca uptake and [Ca2+]i in CGC, and the increase was partially inhibited by NMDARs antagonist, MK-801. This effect was additive to glutamate-induced Ca2+ transients. TBBPA increased oxonol VI fluorescence in CGC reflecting depolarization of the cultured neurons. The binding assays demonstrated potentiation by TBBPA binding of [ 3 H]MK-801 in the presence of NMDA and glycine, with maximum at 20 µM TBBPA, which was inhibited by spermidine and antagonists of the polyamines’ site; inhibition by TBBPA of [ 3 H]glutamate binding, and no significant effect on [3 H]glycine binding. CONCLUSIONS: TBBPA directly enhances the activity of NMDARs in neuronal membranes by interfering with their modulatory sites, and by inducing depolarization of neurons. Supported by the NCN grant 2012/05/B/NZ7/03225
12

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

81%
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.
13

TRP channels participare in memory formation in passive avoidance task in one day old chicks

81%
Salinska E., Stafiej A., Slomka M.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Influx of calcium ions (Ca2+) into neurons after stimulation of glutamate receptors is a crucial step in intracellular cascade of memory formation. Recent findings showed the existence of additional mechanism involved in intracellular Ca2+ increase and triggered not by external signal but by internal signals like increase of Ca2+ within the cell and activation of G protein coupled receptors. We are talking here about transient receptor potential (TRP) channels. The aim of our study was to investigate the participation of TRP channels, especially TRPC and TRPV in intracellular mechanisms engaged in memory consolidation. METHODS: The model of passive avoidance task on one day old chicks was used. Chicks were injected with TRP channels antagonist SKF96365 and three different concentrations of 2-APB, the inhibitor of IP3 receptors, which in small concentrations inhibits also TRP channels. The injections were made at different times before and after training, to find the most effective time of interference. RESULTS: We found that injection of all antagonists immediately after training resulted in task amnesia when tested 24 h later. The amnesic effect of injection of SKF96365 or 2-APB immediately after training was tested at different times. It appeared that SKF96365 injection resulted in constant amnesia that manifested 1.5 h after training, whereas amnesia after injection of 2-APB was observed as early as 30 min after training. The effect of application of TRP channels antagonist SKF96365 on memorizing of the task in comparison with the effects of mGluR1 and mGlR5 antagonists showed similarities when memory was tested 2 h and 24 h training. CONCLUSIONS: Our results show that inhibition of TRP channels results in disturbance in memory formation and that inhibition of both TRP channels and IP3 receptors using small concentrations of 2-APB has a strong impact on this process.
14

Pharmacological profiles of NMDA-induced eicosanoid release in rabbit hippocampus in vivo

81%
Zieminska E., Salinska E., Stafiej A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
15

Inhibition of mGluR5 but not mGluR1 disrupts memory retrieval in the one-trial passive avoidance task in one-day old chicks

81%
Gieros K., Sobczuk A., Salinska E.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
It is known, that group I metabotropic glutamate receptors (mGluRs) are involved in memory consolidation and reconsolidation. The Ca2+ signal derived from IP3 receptors (IP3R) stimulation via mGluRs activation, initiates protein synthesis that is necessary for complete memory consolidation, whereas it is suggested that during retrieval and reconsolidation of memory other mGluR1/5 triggered mechanisms may be involved. Recently mGluRs have received considerable attention as a potential drugs target for many neurological disorders, but their influence on learning and memory is still unclear. With the increasing number of people suffering memory dysfunction of different origin, unravelling of the mGluRs role in memory processes may be very important. The aim of this study was to detect differences in the role for mGluR1 and mGluR5 in memory retrieval at different times after initial training and remainder of the task. One-day old chicks were trained to avoid pecking metal bead covered with bitter-tasting substance methylanthranilate. Two experimental groups were given a reminder by presenting similar metal bead 2 or 24 h after initial training. Bilateral injections of mGluR1 antagonist LY367385 (7.5 nmol/hemisphere), mGluR5 antagonist MPEP (20 nmol/hemisphere) or IP3R antagonist 2-APB (2.5 nmol/ hemisphere) were made directly into the IMM region of chick brain. Injections were made immediately after initial training or reminder, and at 2, 3 and 24 hours later. Our results demonstrate, that in the one-trial passive avoidance task in chicks, injection of the mGluR1 and mGluR5 antagonists into chick brain region IMM shortly after training resulted in permanent amnesia. Injection of MPEP at other times (2, 3 and 24 h after initial training) resulted in transient amnesia observed 1-2 h after injection and lasting up to 4 hours. The same effect was observed for 2-APB. Blocking mGluR1 and mGluR5 immediately after reminder resulted in similar transient amnesia, same as blocking IP3R. Injections of MPEP or 2-APB at later times after reminder also resulted in transient amnesia, however the effect was weaker when reminder was given 24 h after training. mGluR1 antagonist applied later than in a short time after training or reminder had no effect on memory recall. Presented data suggest that at least in the chick model, activation of mGluR1 and mGluR5 is necessary for complete memory consolidation and reconsolidation, whereas mGluR5 are additionally involved in retrieval processes which is dependent on Ca2+ release from IP3 activated intracellular calcium stores.
16

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

81%
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.
17

Prostacyclin reduces early ischemic changes in central nervous system

81%
Pluta R., Salinska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
1990
|
tom 50
|
nr 4-5
18

NMDA - induced processing of beta-APP in hippocampus in vivo and in vitro

81%
Gordon-Krajcer W., Salinska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
19

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

81%
Salinska E., Ziembowicz A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
20

A role for the ryanodine-sensitive intracellular calcium store in long-term memory formation in chick

81%
Salinska E., Bourne R. C., Rose S. P. R.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
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