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1

Synaptosomal transport and metabolism of glutamate precursors in hyperammonemia

100%
Albrecht J., Faff-Michalak M., Hilgier W., Rafalowska U.
Acta Neurobiologiae Experimentalis
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1992
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tom 52
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nr 3
2

L-arginine is an endogenous modulator of cerebral mitochondrial glutamate transport

100%
Dolinska M., Hilgier W., Albrecht J.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
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nr 5
3

Ammonia stimulates glutathione accomulation in the rat cerebral cortex in vivo and in cortical astrocytes in culture

100%
Wegrzynowicz M., Hilgier W., Albrecht I.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
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nr 4
4

Rat cerebral mitochondrial glutaminase activity is unaffected by moderate hyperammonemia in two models

100%
Albrecht J., Hilgier W., Faff L.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 2
5

Prenatal exposure to valproic acid leads to deregulation of purinergic signaling in the brain of adolescent rats

88%
Babiec L., Wilkaniec A., Matuszewska M., Hilgier W., Adamczyk A.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
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nr Suppl.1
Purinergic signaling is involved in many neurodevelopmental alterations that eventually lead to severe disorders, such as autism spectrum disorders (ASD). It was suggested that metabolic pathways that synthesize and catabolize purines are critical regulatory elements in ASD and play a role in promoting behavioral abnormalities. However, the molecular basis of the altered purine metabolism in autism still remains to be elucidated. AIM(S): Investigation the effect of embryological exposure to valproic acid (VPA) – rodent model of environmentally triggered autism – on extracellular nucleotides level and turnover as well as the expression and activity of selected purinergic receptors in the brain cortex of adolescent rats. METHOD(S): Pregnant Wistar rats received a single i.p. injection of VPA (450 mg/kg b.w.) on gestational day 12.5. We isolated CSF and brain cortex from the adolescent (52‑day‑old) male offspring. The experiments were also conducted on primary neuronal cultures isolated from VPA rat pups on the 19th embryonic day. RESULTS: Prenatal exposure to VPA significantly elevated ATP, ADP, and AMP levels in the CSF of adolescent animals, whereas the level of adenosine was unchanged. Concomitantly, cortical expression of ATP hydrolyzing enzymes was significantly decreased. Prenatal exposure to VPA also generated a rearrangement of selected ionotropic and metabotropic purinergic receptors. While the level of purinergic P2X7 and P2Y1 receptors was decreased, the expression of P2X1 receptor was elevated. Additionally, we observed hyperactivity of purinergic receptors in primary neurons isolated from VPA animals. Stimulation of these cells with 1mM ATP induced a 4‑fold increase in intracellular calcium level as compared to control cells. CONCLUSIONS: Prenatal exposure to VPA induces purinergic signaling deregulation in the brain cortex of adolescent offspring and may be involved in the behavioral deficits in ASD. FINANCIAL SUPPORT: Supported by NSC grant 2017/25/B/NZ4/01969.
6

Changes in the content of neuroactive amino acids in cerebral cortical microdialysates of awake and ketamine-anesthetized rats in the asymptomatic stage of thioacetamide-induced hepatic encephalopathy (HE)

88%
Zielinska M., Januszewski S., Hilgier W., Quack G., Albrecht J.
Acta Neurobiologiae Experimentalis
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1999
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tom 59
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nr 3
7

Correlated inhibition of glutamine uptake and phosphate-activated glutaminase activity in rat brain mitochondria by natural and synthetic transport inhibitors

88%
Dolinska M., Hilgier W., Lipkowski A. W., Nowacki J., Albrecht J.
Acta Neurobiologiae Experimentalis
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1999
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tom 59
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nr 3
8

Effect of acute hepatic encephalopathy on [3 H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2plus

88%
Borkowska H. D., Oja S. S., Hilgier W., Saransaari P., Albrecht J.
Acta Neurobiologiae Experimentalis
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2000
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tom 60
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nr 1
Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KC1) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.
9

Glutamate, glutamine and GABA levels in the rat hippocampus in the pharmacological models of autism: a microdialysis study

76%
Diamandakis D., Zieminska E., Hilgier W., Filipkowski R. K., Polowy R., Toczylowska B., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
INTRODUCTION: The disorders of the glutamatergic neurotransmission have been implicated in the pathogenesis of autism, but data on brain content of glutamate (Glu) in patients and animal models are inconsistent. AIM(S): Aim of this study is to evaluate changes in the brain content of Glu, glutamine (Gln) and GABA in the rat models of pharmacologically-induced autism. METHOD(S): The rat females at the 11th day of gestation were given orally 800 mg/kg b.w. of valproic acid (VPA) or 500 mg/kg b.w. of thalidomide (THAL). The pups at PND 9 were submitted to ultrasonic vocalization (USV) test, and at PND 30, under anesthesia, to in vivo unilateral microdi alysis of the hippocampus with a calcium-containing medium. The samples of dialysate representing the basal level followed by a 40 min pulse of 100 mM KCl were collected. The contralateral hippocampi were prepared and homogenized. After derivatization of the amino acids with o-phtalaldehyde, the samples were submitted to HPLC analysis with a fluorescence detection. RESULTS: The results of USV tests showed that the pups prenatally treated with VPA, and to a greater extent with THAL, less frequently produced USV calls, which is regarded as impairment in social communication, a symptom characteristic of autism. In the male rats of the VPA and THAL groups, a total content of Glu increased to 143% and 158%, respectively, and also Gln and GABA contents were significantly elevated. All these values remained unchanged in the female rats. Basal levels of Glu, Gln and GABA in the dialysates of the hippocampi in the experimental groups did not differ from controls, however in VPA‑treated male rats during application of 100 mM KCl a reduction by 59% of Gln concentration and tendency to increase GABA level were found. CONCLUSIONS: The results demonstrate increased content of glutamate in the hippocampus of rats in two chemical models of autism, support a hypothesis on the role of the glutamatergic disturbances in the pathogenesis of autism. FINANCIAL SUPPORT: This study was supported by the Polish National Science Centre, grant no. 2014/15/B/ NZ4/04490.
10

Cytrulina jako parametr prognostyczny całkowitego lub częściowego odstawienia żywienia pozajelitowego u dorosłych pacjentów – obserwacyjne badanie pilotowe

76%
Osowska S., Kunecki M., Hilgier W., Omidi M., Tokarczyk J., Majewska K., Sobocki J.
Diagnostyka Laboratoryjna
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2018
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tom 54
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nr 1
11

Mechanism of ammonia-induced taurine accumulation in the rat striatum in vivo:role of activation of glutamate receptors and ion channels

76%
Zielinski M., Hilgier W., Borkowska H. D., Oja S. S., Saransaari P., Albracht J.
Acta Neurobiologiae Experimentalis
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2001
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tom 61
|
nr 3
12

A link between glutamine metabolism and selective neuronal vulnerability in the hippocampus

76%
Bochomulski P., Krupska O., Klimczak P., Hilgier W., Zablocka B., Beresewicz M.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
|
nr Suppl.1
INTRODUCTION: The brain has developed several endogenous mechanisms to protect itself from the harm ful consequences of ischemia/reperfusion (I/R) injury. Understanding of such mechanisms may be important for the development of new neuroprotective therapies. In a gerbil model of cerebral ischemia, 5 min-ischemia results in selective, delayed neuronal death in the hippocampal CA1 region, while CA2‑4 and the DG remains relatively resistant. We have shown that I/R‑induced translocation of protein kinase C beta II (PKCβII) from cytoplasm to mitochondria only in CA2‑4 and the DG is relevant for ischemia‑resistance of these regions. The exact mechanism remains unknown. AIM(S): The aim of the study was to investigate the role of kidney‑type glutaminase (GLS1), identified as a potential PKCβII partner, in PKCβII‑mediated neuroprotection. METHOD(S): Reciprocal co-immunoprecipitation method showed that of the two GLS1 isoforms, it is GAC not KGA that interacts with PKCβII. In vitro studies revealed that GLS1 may be phosphorylated by PKCβII. GLS1 converts glutamine to glutamate, thus the effect of I/R on activity of GLS1 and level of glutamine and glutamate in mitochondria-enriched fraction were measured. RESULTS: Glutaminase activity is higher in CA2‑4 and DG as compared to CA1 in control and 1 h after I/R, and is confirmed by a reduced level of glutamine in this region. Glutamate level seems to be similar in both regions and is not affected by I/R injury. Application of a selective PKCβII inhibitor increased GLS1 activity in both regions. CONCLUSIONS: This indicates that GAC is not relevant in PKCβII‑mediated neuroprotection, however PKCβII seems to have an influence on the maintenance of glutaminase activity. Moreover, we speculate that ischemia‑resistance of CA2‑4 and the DG is due to its high glutaminase activity, which provides a large amount of glutamate that, in turn, can be effectively used for ATP production in the Krebs cycle or for antioxidant defense based on glutathione synthesis. FINANCIAL SUPPORT: This work was supported by National Science Centre grant 2014/15/D/NZ3/02784.
13

Adaptation of C6 glioma cells to the absence of glutamine in the cultur medium:changes in cell phenotype and glutamine transport characteristics

76%
Dolinska M., Zielinska M., Dybel A., Zablocka B., Buzanska L., Hilgier W., Albrecht J.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
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