Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 40

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Stres, depresja, leki przeciwdepresyjne a plastyczność neuronalna

100%
Nalepa I.
Wszechświat
|
2018
|
tom 119
|
nr 01-03
2

Effects of antidepressants - a focus on the alfa1, adrenergic receptor system

100%
Nalepa I.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
3

O wspolczesnych korzeniach chorob neurodegradacyjnych

100%
Nalepa I.
Wszechświat
|
2002
|
tom 103
|
nr 01-03
14-21
4

Cellular and molecular aspects of depression

100%
Nalepa I.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
5

Krotko o rzeczach waznych w zyciu komorki czyli bialkowa kinaza C i jej rola w mechanizmie przetwarzania sygnalu blonowego

100%
Nalepa I.
Wszechświat
|
1997
|
tom 98
|
nr 05
115-117
6

Funkcjonowanie mozgu a zdrowy tryb zycia

75%
Nalepa I.
Wszechświat
|
2009
|
tom 110
|
nr 01-03
33-39
7

O tym jak komorka kontaktuje sie ze swiatem zewnetrznym i co z tego wynika

75%
Nalepa I.
Wszechświat
|
1992
|
tom 93
|
nr 02
37-40
8

Second messengers: rate of formation as an index of receptor reactivity

63%
Nalepa I., Vetulani J.
Acta Neurobiologiae Experimentalis
|
1990
|
tom 50
|
nr 6
9

Similar action of the ECS and imipramine chronic treatments on subtypes of the alfa1 adrenoceptor

63%
Nalepa I., Kreiner G.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
10
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Sirtuiny - intrygujące wielozadaniowe "strażniczki" procesów życiowych

63%
Bielawski A., Nalepa I.
Wszechświat
|
2019
|
tom 120
|
nr 04-06
11

In vitro effects of antidepressants on noradrenaline-dependent second messenger systems

63%
Nalepa I., Vetulani J.
Acta Neurobiologiae Experimentalis
|
1992
|
tom 52
|
nr 3
12
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Lepiej poznać, by lepiej leczyć - zwierzęce modele stwardnienia rozsianego

63%
Jankowska M., Nalepa I.
Wszechświat
|
2018
|
tom 119
|
nr 10-12
13

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

51%
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.
14

Elevated expression of HSP72 mRNA in the prefrontal cortex of rats nonresponding to imipramine treatment in the chronic mild stress model of depression

51%
Bielawski A., Papp M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
15

Depletion noradrenaline counteracts the increase of alpfaIA-adrenoceptor mRNA expression induced by treatment with antidepressant

51%
Kreiner G., Zelek-Molik A., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
16

Differential mRNA expression level of the Bcl2 protein family in the thalamus of rats reactive and non-reactive to chronic mild stress - the animal model of depression

51%
Bielawski A., Rafa-Zablocka K., Papp M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Apoptosis is controlled by the balance between pro- (Bax) and anti-(Bcl-2, Bcl-xl) apoptotic proteins within the cell. Bcl-2 and Bcl-xl interact with Bax in the outer mitochondrial membrane and regulate the release of cytochrome c, which activates caspases, the main executors of apoptosis. The increased ratio of pro- vs. antiapoptotic proteins is associated with an enhanced vulnerability to apoptotic activation. The chronic mild stress (CMS) procedure induces depression-like symptoms in animals. The rats subjected for a prolonged period of time to a variety of mild stressors gradually decrease their responsiveness to rewarding stimuli (e.g., consumption of sweet pellets). We aimed to investigate the expression of Bcl-2, Bcl-xl and Bax mRNAs in the thalamus of rats subjected to the 3-weeks CMS. Three groups of male Wistar rats, selected basing on behavioral test of sucrose (1% solution) consumption – sham, stress reactive and stress non-reactive, were considered. The mRNA expression was measured by quantitative RT-PCR applying TaqMan probes. We found that in the thalamus of rats developing anhedonia to sucrose consumption after the CMS, the mRNA expression of both anti-apoptotic (Bcl-2 and Bcl-xl) and pro-apoptotic (Bax) genes was significantly attenuated, though to a various extent. In the stress reactive animals, the Bcl-2 mRNA was decreased by 57% (p<0.01), Bcl-xl – by 51% (p<0.05) and Bax – by 24% (p<0.05), while no change was noticed in the stress non-reactive animals. Further analysis revealed a significant decrease in the Bcl-2/Bax and Bcl-xl/Bax ratios (respectively, by 48% and 25%; p<0.01) in the stress reactive animals, and no change in case of the stress non-reactive animals. Our results suggest that the behavioral reactiveness of rats to the CMS is associated with the enhanced susceptibility to apoptotic activation and development of apoptotic processes in the thalamus. Supported by statutory funds of the Institute of Pharmacology, PAS.
17

Involvement of non-receptor protein kinases in the mechanism of imipramine action

51%
Zalewska T., Zajac H., Bielawski A., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
Chronic treatment with antidepressant imipramine increases synaptic plasticity and connectivity in the rat brain. Signals that orchestrate changes associated with neuronal plasticity derive in part from extracellular matrix (ECM). Two homologous tyrosine kinases ñ FAK and PYK2 are thought to play a major role in transducing signals from extracellular matrix to the cell interior. This prompted us to examine the effect of acute and chronic imipramine treatment on the activity of FAK and PYK2-dependent signaling pathway in the rat brain cortex. To approach this problem we aimed to quantify the level of FAK and PYK2 phosphorylation of their tyrosine residues as well as interaction of these kinases with downstream signaling substrates such as the Src kinase, adaptor protein p130Cas, and cytoskeletal protein-paxilin. Our results demonstrate different responses of the two kinases to the imipramine administration. Imipramine leads to the suppression of FAK-dependent pathway with simultaneous stimulation of the pathway coupled with PYK2 kinase. The reduction in FAK Tyr 397 phosphorylation, in particular after chronic administration of the drug, was translated into a decreased association of FAK with downstream molecular partners, Src kinase and p130Cas. In contrast, the acute and chronic treatment with imipramine leads to activation of 402 tyrosine phosphorylation of PYK2 kinase and in consequence increased interaction with kinase Src and adaptor protein p130Cas. Because both kinases appear to be well suited to play a role in synaptic plasticity, it seems probably that PYK2 may function in a compensatory manner for the FAK inhibition and may be responsible for neuronal plasticity-connected events after imipramine treatment. Supported by Polish MNSW Scientifi c Network Fund
18

Imipramine-induced changes in expression of G proteins and ERKs in cerebral cortex of rat

51%
Wieczorek K., Bielawski A., Zalewska T., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
Imipramine belongs to a class of tricyclic antidepressants which augment monoaminergic transmission in a brain and are prevailingly used in treatment of depressive disorders. Increased availability of neurotransmitters (e.g., noradrenaline and serotonin) results among others, in modulation of the activity of G protein-coupled receptors and other proteins involved in intracellular signaling. The study was aimed to assess the effects of single and repetitive treatment with imipramine (10 mg/kg, twice daily, for 21 days) on the expression of G11, GQ and G12 proteins and protein kinases, ERK1/ERK2 and pERK1/pERK2 in the rat prefrontal cortex. Animals were sacrifi ced 4 and 24 h after the last drug injection. Single and chronic treatments with imipramine decreased similarly the Gq protein level (by 29, 36 and 48%), while G11 and G12 were unchanged. In contrast, the acute imipramine dose increased the level of ERK1 (by 32% above saline control) that was further enhanced by the chronic treatment (by 48% and 64%, respectively). The increase in ERK2 level was similarly marked (at both time-points) after chronic (by 39% and 31%) and after single dose of drug (by 28% vs. saline). Interestingly, the ERK1/ERK2 ratio was changed only at 24 h after completion of chronic treatment (127% vs. saline control). The same direction of changes, independently on amount of imipramine doses, was observed in the case of pERK1 and pERK2 (increase by approx. 25% of saline group). Our data demonstrate that treatment with imipramine causes downregulation of Gq protein level and upregulates the ERK1/ERK2 pathway(s). The results suggest that imipramine-induced changes in ERKs can result from other than Gq-linked intracellular signaling. Supported by Polish MNSW Scientifi c Network fund.
19

Evaluation of transgenic mice conditionally lacking CREB in noradrenergic neurons as a novel tool for studying its role in the antidepressant drug action

51%
Rafa-Zablocka K., Kreiner G., Baginska M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Most of the current antidepressants modulate levels of monoamines just after administration, however, only after prolonged therapy the clinical effect may be observed. Myriad attempts tried to identify molecular factors responsible for such a delayed response, the prominent example being the cyclic AMP response element binding protein (CREB). Many research suggest that chronically given antidepressants enhance CREB levels and activity. On the other hand, CREB knock-out mice showed rather antidepressant-like behavior, however, the compensatory effects of cAMP response element modulator (CREM) in absence of CREB were not taken into account. In our study we evaluated transgenic mice with selective ablation of CREB in noradrenergic cells, maintained in CREM deficient background (CrebDBHCreCrem-/-) for elucidation of the role of CREB in antidepressant treatment. METHODS: mRNA levels of neurotrophins and α1-adrenoceptors in CrebDBHCreCrem-/- mice were investigated in hippocampus and prefrontal cortex using qPCR method. Next mice were screened in behavioral tests like: open field (OF), tail suspension test (TST) and rotarod. Preliminary TST after acute desipramine (DMI) administration (20 mg/kg, ip) was executed. RESULTS: CrebDBHCreCrem-/- mutant mice did not show any abnormalities in their basal phenotype, moreover the mRNA levels of studied genes were not changed either. However, preliminary experiments revealed that CrebDBHCreCrem-/- show a treatment-resistant phenotype after acute DMI administration in TST, (effect absent in single mutants). CONCLUSIONS: Our results provide further evidence for the important role of CREM as a compensatory factor and indicate that these mice may represent an unique tool to dissect the role of CREB in the mechanism of antidepressants. Supported by statutory funds of the Institute of Pharmacology and 2014/13/B/NZ7/02293 grant. K. Rafa-Zabłocka is a holder of scholarship from the KNOW sponsored by MSHE, Poland.
20

Effects of some environmental components of air pollution on selected parameters of metabolic activity of neuronal and macrophagal cells in context of potential role in a pathomechanism of neurodegenerative disorders

51%
Roman A., Jankowska M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: A number of literature reports pointed out a connection between neurodegenerative disorders morbidity and air pollution with particulate matter (PM) containing transition metals. PM exerts their effect by activation of immune system and oxidative stress induction. AIM(S): The aim of this study was to assess whether exposure to PM is associated with proinflammatory activation of macrophagal cells and negative neuronal cells condition including reactive oxygen species (ROS) generation. METHOD(S): Particulate matter NIST1648A (standard material) and LAp120 (NIST1648A devoid of organic components) were investigated for their biological potency in mouse macrophagal cell line RAW 264.7 and in human neuronal cell line SH-SY5Y. It was assessed using metabolic activity assay (resazurin reduction (RES) test), ROS generation assay (DCFH-DA test), nitric oxide (NO) synthesis and superoxide anion (O2-) release (NBT reduction test). RESULTS: At highest concentration (100 μg/ml) and longest incubation time (48 h), NIST1648A slightly increased metabolic activity, NO synthesis and O2-release in macrophagal cells. In these conditions LAp120 decreased metabolic activity and O2‑release without influence of NO synthesis. Both forms of PM shortly increased the ROS generation. In neuronal cells both forms of the PM resulted in increase of ROS generation and decreased metabolic activity. CONCLUSIONS: The PM tested in this study possess a potential to direct activation of innate immunity and to direct damage of neuronal cells probably by oxidative stress induction. FINANCIAL SUPPORT: The study was supported by APARIC project – NCN grant No. 2015/16/W/ST5/00005, and statutory funds of Institute of Pharmacology Polish Academy of Sciences.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.