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1

Rynek opakowan i materialow opakowaniowych w Polsce

100%
Kusmierczyk J.
Opakowanie
|
1995
|
nr 1
32-33
2

Intraperitoneal delivery of ex vivo activated macrophages results in depression-like behavior of mice

81%
Roman A., Kusmierczyk J., Klimek E., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Excessive pro-inflammatory activity of macrophages is regarded as one of pathomechanisms of depressive disorders. Administration of lipopolysaccharide (LPS) induces potent activation of whole immune system and is used as an animal model of depression. In this study we investigated whether macrophages, previously activated ex vivo and delivered to mice, are able to induce the behavioral changes related to depression. The experiment was carried out on male C57BL/6J mice. Peritoneal macrophages were stimulated in vitro with LPS for 3 h. Then they were stained with 5(6)- carboxyfluorescein diacetate N-succinimidyl ester and injected intraperitoneally at the dose of 2×106 cells per mouse. Control group was administered likewise with non-stimulated cells. Twenty hours later the recipients were subjected to tests of depressive-like behavior including the locomotor activity, the tail suspension test and the forced swimming test (FST). Presence of injected cells in various compartments of the body was assessed 28 h after administration using flow cytometry and fluorescence microscopy. We found that the administration of ex vivo activated macrophages caused a decrease of initial exploratory activity of the mice (by 26%) and decreased struggling behavior in the FST (by 65%) in comparison to animals administered with non-stimulated cells. Majority of administered macrophages went away from the peritoneum. They were absent in spleen, in lymph nodes and in pleural cavity but were present in blood. Activated macrophages were more mobile than non-stimulated cells (below 1% and about 5% of peritoneal cells, respectively). These results suggest that ex vivo activated macrophages are able to change some parameters of recipients’ behavior in depressive-like fashion. The fate of activated cells varies as they are more mobile in the recipients’ body as compared with non-activated cells. Supported by a grant POIG.01.01.02-12-004/09-00 financed by European Regional Development Fund.
3

The lack of glucocorticoid receptor on noradrenergic cells does not influence an inflammatory response after chronic stress

71%
Kusmierczyk J., Chmielarz P., Trojan E., Roman A., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Noradrenergic neurons with terminals in the hypothalamus are known to regulate activity of the hypothalamic pituitary adrenal (HPA) axis. The aim of the study was to evaluate whether glucocorticoid receptor (GR) ablation in noradrenergic cells affects the inflammatory response in the central nervous system (CNS) and functioning of immune organs under chronic restraint stress (CIS) conditions. METHODS: Selective ablation of GRs in the noradrenergic system (GRDBHCre mice) was achieved using the Cre/loxP approach. The male mice were kept in standard laboratory conditions. The CIS procedure was performed by placing animals, for 2 hours daily, in 50 ml disposable centrifuge tubes and was repeated for 14 days The expression of cytokines in selected brain structure was analyzed with TaqMan RT-PCR assay. The relative thymus and spleen mass were calculated as well as peritoneal cell ability to production of selected cytokines after stimulation. RESULTS: We found that CIS procedure caused the decrease in body and relative thymus weights in both wt and mutant mice. The mRNA expression of interferon gamma and interleukin-6 genes was elevated in the hypothalamus, prefrontal cortex and hippocampus in mutation independent manner. We also found the increase in production by peritoneal macrophage cells on tumor necrosis factor alpha and interleukin 1beta after pro-inflammatory stimulation and increase in interleukin 4 productions in anti-inflammatory stimulation in both wt and mutant mice. CONCLUSIONS: The regulation of inflammatory process is a complex process in which a number of cells and molecules play different roles in a coordinated and well-controlled manner. Therefore, the lack of GR in noradrenergic cells might be too subtle and insufficient modification to cause disturbances in inflammatory responses after chronic stress. Supported by grant no. POIG.01.01.02-12-004/09 co-financed by the ERDF and by statutory funds of Institute of Pharmacology PAS.
4

Effects of bi-adrenergic receptor blockade during chronic restraint stress on the expression of selected proteins of the glutamatergic transmission in the rat prefrontal cortex

61%
Zelek-Molik A., Kowalska M., Roman A., Kusmierczyk J., Bielawski A., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: The stress impaired the structure and activity ofthe prefrontal cortical(PFC) neurons has been postulated to underlie the pathology of stress related psychiatric disorders. NMDA and AMPA glutamate receptors of PFC were shown to be affected by stress. High level of the noradrenaline release during stress is known to stimulate the β adrenergic receptors (βAR), densely expressed in PFC. The βAR can directly or indirectly, by means of Fyn kinase, regulate glutamatergic receptors activation. Also, evidence have shown that pharmacological blockade of β1AR alleviated anxiety in stress models. The aim of the study wasto evaluate the stressinduced changes in the expression of total- and phospho-(Y1472)GluN2B, (Ser845)GluA1, and (Y530)Fyn proteins in rat dorso-medial (dm) PFC and to assess whether β1AR blockade can modulate it. METHODS: Male Wistar rats underwent the chronic restraint stress procedure applied for 3 hours daily, for 14 days. During the last 7 days rats were treated with betaxolol (1 or 5 mg/kg/po) given immediately after daily stress. Next day after a completion of stress procedure, the rats were decapitated, their dmPFC was dissected and subjected to standard Western blot analysis. RESULTS: Neither stress nor betaxolol treatment changed the expression of studied NMDA and AMPA subunits. Repeated stress increased phosphorylation level of (Y530)Fyn kinase (by 25% vs. non stressed groups) and betaxolol treatment did not influence this effect. CONCLUSIONS: The Fyn kinase is a known regulator of NMDA receptors’membrane stability, on the other hand phosphorylation at Tyr 530 inactivates the kinase. Our results showing the increased phosphorylation of Fyn suggest the inhibition of Fyn activity which can be responsible for disturbed glutamatergic transmission observed in PFC after prolonged stress. This mechanism seems to be independent on β1AR activity in PFC. Supported by statutory funds of the Institute of Pharmacology PAS.
5

The influence of conditional inactivation of GR in noradrenergic system on stress related behavior in mice

61%
Kreiner G., Chmielarz P., Kusmierczyk J., Parlato R., Schuetz G., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Depression is a mental disease affecting complex cognitive and emotional functions. Stress induced hyperactivity of hypothalamic-pituitary-adrenal system (HPA) is believed to be one of the major contributors to its pathology. The activity of HPA is controlled by glucocorticoid receptors (GR) which function may be impaired in depression, resulting in reduced GR-mediated negative feedback on the HPA-axis. Most of the compounds which modulate GR action also influence noradrenergic system by increasing noradreneline levels. The aim of this study was to investigate if conditional inactivation of GR in noradrenergic neurons of mice affects the animal behavior in stressful conditions. Selective ablation of GR in noradrenergic system was achieved using the Cre/loxP approach by crossing transgenic mice hosting the Cre recombinase under the dopamine beta-hydroxylase (DBH) promoter with animals harboring the floxed GR gene. Resulting GRDBHCre mutant mice were born at expected rates, viable and showed no obvious physical impairment regarding life span, weight gain and locomotor activity. Also plasma cortisol levels did not differ between mutant and control mice. Animals were screened for anxiety and depressive-like behavior in light/ dark box test (LDT) and tail suspension test (TST). Male mutant mice did not unveil any differences from their control littermates in basal state nor after acute restraint stress (2 hrs). However, both tests performed after chronic restraint stress (14 days, 2 hrs/day) revealed that GRDBHCre mice were resistant to this type of experimental procedure showing similar anxiety status and immobility time as non-stressed controls. Our mutant mice may represent an interesting tool to study the role of stress in depression in context of noradrenergic system which is important target for antidepressant therapy. This study was supported by grant POIG.01.01.02-12-004/09 (DeMeTer) financed by European Regional Development Fund.
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