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1

'Blaski i cienie' wykorzystywania genow metabolizmu podstawowego jako genow kontrolnych

100%
Bielawski A.
Wszechświat
|
2002
|
tom 103
|
nr 07-09
190-193
2

Glutamate dehydrogenase and glutamine synthetase in rye seedlings supplied with ammonium and nitrate

63%
Bielawski W., Bielawski A.
Acta Biochimica Polonica
|
1979
|
tom 26
|
nr 4
3
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Sirtuiny - intrygujące wielozadaniowe "strażniczki" procesów życiowych

63%
Bielawski A., Nalepa I.
Wszechświat
|
2019
|
tom 120
|
nr 04-06
4

Idealna terenówka myśliwska

63%
Bielawski A.
Brać Łowiecka
|
2009
|
nr 07
5

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
6

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.
7

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
8

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.
9

Elevated expression of alpha1-adrenoceptor subtypes in the hippocampus of rats non-responding to imipramine treatment in the chronic mild stress

51%
Bielawski A., Kowalska M., Papp M., Nalepa L.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Cerebral α1-adrenoceptors (α1-AR) are known to be changed by stress conditions and involved inthe mechanism of antidepressant action. The chronic mild stress (CMS) procedure that induces depression-like symptoms in animals is a useful tool to study the mechanisms of action of antidepressant drugs in animals. We aimed to investigate the expression of α1A-, α1B-, and α1D-AR mRNAs in the hippocampus of rats subjected to the standard CMS procedure and then treated with an antidepressant drug, imipramine (IMI). Five groups of male Wistar rats were considered in the study: sham-saline; stress-saline; sham-IMI; stress-IMI and IMI-non-responders (i.e., stressed rats, which did not respond to IMI treatment). The expression of α1-ARs was measured at the level of mRNA (by quantitative real-time PCR) and their total density analyzed by [3H]prazosin autoradiography. We found that both CMS procedure and IMI-treatment did not affect the expression of all α1-AR mRNAs. However, in rats non-responding to IMI treatment in behavioral test, the expression of α1A- , α1B- and α1D-AR mRNAs was signifi cantly increased (respectively, by 81%, P<0.01 78%, P<0.01; 46%, P<0.5) compared to sham-saline and stressIMI groups. Similar direction of change was seen in α1-AR total density. Our results suggest the involvement of all subtypes of α1- adrenoceptor in the phenomenon of resistance of depressive animal to IMI treatment. Supported by statutory funds of the Institute of Pharmacology, PAS.
10

Changes in mRNA expression of alpha1-adrenoceptor subtypes in brain of rats reactive to the chronic mild stress

51%
Bielawski A., Zablocka K., Papp M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
The chronic mild stress (CMS) procedure induces depression-like symptoms in animals. In this model of animals’ depression, 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). Cerebral alpha1-adrenoceptors (alpha1-AR) are known to be essential for behavioral activation in rodents and changed by stress conditions. Molecular and pharmacological studies revealed the existence of three subtypes of alpha1-AR, named alpha1A, alpha1B and alpha1D. These alpha1-ARs are widely expressed in the brain, though the functional differences among individual subtypes are not clear. We aimed to investigate the expression of alpha1A-, alpha1B- and alpha1D-AR mRNAs in the thalamus, the hippocampus and the prefrontal cortex of rats subjected to the standard CMS procedure. Three groups of male Wistar rats were selected based on behavioral test of sucrose (1 % solution) consumption and were considered in the molecular study: sham, stress reactive and stress non-reactive in the behavioral test. The expression of alpha1-AR mRNAs was measured by quantitative real-time PCR method with the use of TaqMan probes. We found that CMS procedure differently affected the expression of the alpha1-AR mRNAs and the changes were brain structureand receptor subtype-dependent. No changes in expression of three subtypes of alpha1-AR mRNAs was found in the prefrontal cortex. In the thalamus of rats that developed anhedonia to sucrose consumption after the CMS, the expression of all alpha1-AR subtypes was significantly attenuated: the alpha1A mRNA was decreased by 52%, alpha1B - by 55% and alpha1D - by 57% (p<0.05) in the stress reactive animals, while no change in the alpha1-ARs expression was observed in the stress non-reactive animals. In the hippocampus, an opposite direction of change was observed and the effect was limited to the alpha1B-AR mRNA which was increased in the stress reactive group of animals (by 128 %, p<0.5, vs. sham group). Similarly to the thalamus, the alpha1-ARs level in the hippocampus was unchanged in the group of stress non-reactive animals. Our results indicate that CMS induces changes in all subtypes of thalamic alpha1-ARs and suggest the significant impairment of noradrenergic transmission in the thalamus of stress reactive rats. In addition, the hippocampal alpha1B receptor seems to be specifically involved in the phenomenon of response of animals to CMS. Supported by a grant POIG.01.01.02-12-004/09-00 financed by European Regional Development Fund.
11

Zastosowanie kleju fibrynowego w operacjach u malych zwierzat

45%
Szponder T., Brodzki A., Orzelski M., Polkowska I., Bielawski A.
Magazyn Weterynaryjny
|
2006
|
tom 15
|
nr 01
30
12

Changed expression of apoptotic signaling-releted genes, Pmaip1 and Rock1, in the prefrontal cortex of rats treated with imipramine in chronic mild stress model of depression

45%
Bielawski A., Rafa-Zablocka K., Zelek-Molik A., Papp M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: The chronic mild stress (CMS) procedure induces depression-like symptoms in animals. In this model, rats subjected for a prolonged time to mild stressors gradually decrease their responsiveness to rewarding stimuli. This deficit can be effectively reversed by chronic antidepressant treatment. Apoptotic changes in the prefrontal cortex were shown in animal stress models, as well as degenerative changes, which are reversed by antidepressant treatment in depressed patients. We aimed to study the apoptotic signaling-related genes in the prefrontal cortex (PFC) of rats treated with imipramine (IMI) in CMS model. METHODS: First, we used the TaqMan Low Density Arrays to indentify genes in the three groups of Wistar rats: sham-saline; stressIMI-responders and stress-IMI-nonresponders (the sucrose intake score did not return to the control level). Then, these groups of rats and two additional ones (stress-saline and sham-IMI) were assessed in the PCR reactions with one TaqMan probe for detailed mRNA analysis of the identified genes. Finally, the levels of these proteins were assessed by Western Blot in all experimental groups. RESULTS: We found that CMS decreased the expression of Pmaip1 mRNA (by 18%) and the effect remained unchanged in rats nonresponding behaviorally to IMI treatment. Furthermore, in rats nonresponding to IMI treatment, the Rock1 mRNA was decreased by 40% vs. sham and IMI responding rats. However, at the Rock1 protein level its decreased expression was observed in both groups, the IMI nonresponding and IMI responding animals (by 22% and 29%, respectively). CONCLUSION: Our results suggest the involvement of apoptotic Pmaip1 and Rock1 genes in the process of response to IMI treatment in CMS model of depression in rats. Supported by statutory funds of the Institute of Pharmacology PAS and POIG.01.01.02-12-004/09-00 grant financed by European Regional Development Fund.
13

Imipramine-reversed elevation of Hsp72 expression in the brain of rats in the chronic mild stress model of depression

45%
Bielawski A., Zelek-Molik A., Papp M., Kowalska M., Nalepa L.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Heat shock proteins HSP70 play a protective role against stressinduced damage of cells. We assessed the expression of inducible Hsp72 in the prefrontal cortex (PFC) and hippocampus (HIP) of male Wistar rats subjected to the chronic mild stress (CMS), the procedure inducing depression-like symptoms, and subsequently Different brain areas are thought to be integrated into largescale networks. Recent approaches for investigating structural organization and functional coordination within these networks involve measures of connectivity among brain areas. Transcranial magnetic stimulation (TMS) can be used to analyze the functional state of the cerebral cortex, discovering changes in its excitability, connectivity and plasticity which may have occurred through processes such as learning or recovery from a lesion. We review studies using in vivo functional brain connectivity technologies. TMS-EEG studies have begun to describe the nature of the TMS-evoked EEG responses in order to broaden the comprehension of the activation mechanisms of TMS. Several studies have proved the power of TMS-EEG by displaying many data about the excitability or connectivity of the brain. Particularly, it has been proposed that the very first part of the TMS evoked EEG response displays the excitability of the stimulated cortex while its spatio-temporal distribution over the scalp displays the spread of activation to other cortical areas – via intra and inter-hemispheric cortico-cortical connections as well as to sub-cortical structures and spinal cord via projection fibres – that means the effective connectivity of the stimulated area. Finally effective connectivity may be considered as the union of structural and functional connectivity. These studies provide insights into the relationships between brain structure and function.
14

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

39%
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.
15

Changes in alfa1-adrenergic receptor subtypes in the hippocampus of rats non-responding to imipramine treatment in the chronic mild stress model of depression

39%
Rafa-Zablocka K., Zelek-Molik A., Bielawski A., Gruca P., Lason-Tyburkiewicz M., Papp M., Nalepa I.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Despite many years of research on depression the mechanism of the disorder remains elusive. Many studies are focused on dysfunction of central monoaminergic systems and some evidence exist for the role of α1-adrenoceptor (α1-AR). There are three subtypes of this receptor - α1A, α1B and α1D, which are widely distributed in brain. The aim of this study was to assess the expression of all three α1-AR, both at the mRNA and at the protein level in the hippocampi of male Wistar rats, subjected to the chronic mild stress (CMS) procedure followed by treatment with antidepressant drug, imipramine (IMI). Five groups of animals were studied: sham-saline; stress-saline; sham-IMI; stress-IMIresponders and stress-IMI-non-responders. The latter included the stressed animals resistant to IMI treatment as indicated by anhedonia test. The mRNA level was measured using qRT-PCR and SybrGreen dye, and the protein level was assessed by Western blotting. We found that mRNA expression of all α1-AR subtypes was significantly elevated only in the IMI-non-responders group (α1A-AR by 76%; α1B-AR by 96%; α1D-AR by 50%, vs. shamsaline). Moreover, stress alone caused an increase in α1A-AR mRNA (by 41%) though the effect was statistically insignificant. Changes found in the protein level were less pronounced. The only difference between IMI-responders and non-responders was found in α1A receptor protein that was decreased by 73% vs IMIresponders. The level of α1D protein was elevated in all IMI treated groups (by about 79%, vs. sham-saline) and the change occurred independently on stress procedure. No change in the α1B protein was found. Our results indicate that although α1A-AR and α1D-AR are involved in mechanism of IMI action, only the α1A receptor seems to be engaged in the phenomenon of resistance to IMI treatment. Supported by a grant POIG.01.01.02-12-004/09-00 financed by European Regional Development Fund.
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