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1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Stres a depresja

100%
Budziszewska B.
Wszechświat
|
2016
|
tom 117
|
nr 01-03
2

Specific binding sites for progesterone and 17beta-estradiol in cells of Triticum aestivum L.

51%
Janeczko A., Budziszewska B., Skoczowski A., Dybala M.
Acta Biochimica Polonica
|
2008
|
tom 55
|
nr 4
707-711
The presence and location of specific binding sites for progesterone and 17β-estradiol in cells of wheat were estimated using radioligand binding assay. Membrane and cytosolic fractions of non-vernalized and vernalized plants were tested using tritium-labelled ligands. Specific binding of [3H]progesterone and [3H]17β-estradiol occurs in wheat cells. The binding sites are located in membranes and in the cytosol. Specific binding of [3H]17β-estradiol is higher in the membranes than in the cytosol. Specific binding of both ligands in the cytosolic fraction is higher in vernalized plants than in non-vernalized ones. The possibility of the occurrence of steroid binding proteins specific for progesterone and 17β-estradiol, putative steroid receptors for these steroids in Triticum aestivum L., is discussed.
3

The effect of chronic cocaine "binge" administration on [3H] dopamine uptake in the nucleus accumbens and striatum of the rat

51%
Jaworska-Feil L., Budziszewska B., Lason W.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
4
Content available remote

Excitatory neurosteroids attenuate apoptotic and excitotoxic cell death in primary cortical neurons

51%
Leskiewicz M., Jantas D., Budziszewska B., Lason W.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 3
457-475
Some neurosteroids show neuroprotective action in in vitro and in vivo studies, but their interaction with apoptotic/necrotic processes has been only partially unraveled. The aim of the present study was to examine the effect of dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), pregnenolone (PGL) and allopregnanolone (Allo) on staurosporine-, glutamate-, and NMDA-induced damage in primary cortical neuronal culture. DHEA, DHEAS and PGL (0.1 and 1 µM) inhibited the staurosporine-evoked LDH release and decreased the number of apoptotic cells as shown by Hoechst`s staining, whereas Allo was without effect. The neurosteroids affected neither the staurosporine-evoked changes in caspase-3 activity nor the decrease in mitochondrial membrane potential. It was also shown that protective effects of DHEA, DHEAS and PGL against staurosporine-induced LDH release were attenuated by extracellular signal-regulated kinase (ERK) - mitogen-activated protein kinase (MAPK) inhibitor – PD 98059 (5 µM) but not by phosphatidylinositol-3-kinase (PI3-K) inhibitors such as LY 294002 (1 µM) or wortmannin (10 nM). The involvement of ERK2-MAPK in protective effects of neurosteroids was confirmed by Western blot study. Further study demonstrated that glutamate-induced cell damage was attenuated by DHEA, DHEAS, and PGL, but not by Allo. None of the steroids influenced NMDA-induced LDH release. The results of the present in vitro studies suggest that excitatory neurosteroids DHEA, DHEAS and PGL at physiological concentrations participate in the inhibition of cortical neuronal degeneration elicited by staurosporine and glutamate, whereas the most potent positive modulator of GABAA receptor - Allo - has no effect. Moreover, neurosteroids appear to attenuate the staurosporine-induced cell damage in a caspase-3 independent way and their neuroprotective mechanism of action involves the increase in ERK-MAPK phosphorylation.
5

Problemy żywienia w przebiegu transplantacji szpiku kostnego

51%
Budziszewska B., Rzepecki P., Sulek K., Klos M.
Żywienie Człowieka i Metabolizm. Suplement
|
2000
|
tom 27
274-278
6

Effects of neurosteroids on apoptotic processes in neuronal cells in vitro

51%
Lason W., Leskiewicz M., Budziszewska B., Regulska M.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
7

The effect of repeated amphetamine administration on steroid hormone levels in the rat plasma

51%
Budziszewska B., Jaworska-Feil L., Lason W.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
8

The effect of antidepressant drugs on glucocorticoid receptor-mediated gene transcription in the presence of Iow and high concentration of corticosterone

51%
Olczyk M., Budziszewska B., Jaworska-Feil L., Lason W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Effects of 17-beta estradiol and estriol on NMDA-induced toxicity and apoptosis in primary cultures of rat cortical neurons

51%
Kajta M., Budziszewska B., Marszal M., Lason W.
Journal of Physiology and Pharmacology
|
2001
|
tom 52
|
nr 3
10
Content available remote

Effect of allopregnanolone on D-[3H]-aspartate release and [3H]-glutamate uptake in the hippocampus of kainate-treated mice

51%
Leskiewicz M., Budziszewska B., Jaworska-Feil L., Lason W.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 2
In order to determine whether the status epilepticus leads to alterations in the neurosteroid effect on excitatory amino acid transmission, we studied the influence of allopregnanolone on aspartate release and glutamate uptake in mouse hippocampus at various times after kainate administration. No significant differences in the K+-stimulated D-[3H]-aspartate release from the hippocampi of saline- and kainate-treated mice were observed; however, that parameter tended to fall in tissues collected 1h after kainate administration. Allopregnanolone significantly attenuated the K+-stimulated D-[3H]-aspartate release from the hippocampi of control animals, as well at 24 h and 7 days after kainate injection; in contrast it did not affect amino acid release from the hippocampi collected 1 h after kainate administration. Kainate administration had no effect on [3H]-glutamate uptake after 1 and 24 h, but elevated that parameter on day 7. Allopregnanolone (10 and 100 µM) did not affect [3H]-glutamate uptake in control and kainate-treated mice. In conclusion, the present study indicates a loss of the inhibitory effect of allopregnanolone on the potasium-stimulated D-[3H]-aspartate release from mouse hippocampus during the kainate-induced status epilepticus; moreover, it excludes involvement of this neurosteroid in the regulation of hippocampal [3H]-glutamate uptake in both control and kainate-treated mice.
11

Inhibitory effect of antipsychotic drugs on the human corticotropin-releasing-hormone gene promoter activity oper-ate through a PI3-K/AKT mediated pathway

45%
Basta-Kain A., Budziszewska B., Jaworska-Feil L., Tetich M., Lason w.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
12

Effect of combined treatment with imipramine and amantadine on the pharmacokinetic and endocrine parametrs of rats subjected to the forced swimming test

39%
Rogoz Z., Budziszewska B., Daniel W. A., Kot M., Wojcikowski J., Maj J.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
13

The effect of TRH and its analogs on hydrogene peroxide-induced toxicity in differentiated human neuroblastoma SH-SY5Y cells

39%
Jaworska-Reil L., Budziszewska B., Leskiewicz M., Regulska M., Lipkowski A. W., Lason W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
14

Effects of neurosteroids on neuronal survival: Molecular basis and clinical perspectives

39%
Leskiewicz M., Budziszewska B., Basta-Kaim A., Zajac A., Kacinski M., Lason W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
Neurosteroids have long been known to act as important modulators of central nervous system functions. The concept of their mechanism of action, however, have essentially undergone an evolution. Previously, these compounds were postulated to regulate neuronal function mainly via allosteric regulation of some membrane-bound receptors, such as GABAA and NMDA receptors, in a non-genomic way. Recent studies have provided evidence for intracellular targets for neurosteroids, e.g., transcription factors (NFk-B, progesterone receptors), protein kinases (phosphatidylinositol 3-kinase, protein kinase C), or microtubule-associated proteins, i.e. factors essential in regulation of neuronal survival and apoptosis. This paper reviews in vitro and in vivo data on neurosteroid involvement in the regulation of neurodegenerative processes with emphasis on new intracellular and genomic mechanisms of their action. Potential utility of neurosteroids in the treatment of some neurodegenerative disorders has been also discussed.
15

Brain level of FKBP-51, a glucocorticoid receptor cochaperone, is decreased in a neurodevelopmental animal model of schzophrenia

39%
Basta-Kaim A., Budziszewska B., Kabera M., Leskiewicz M., Regulska M., Korzeniak B.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Recent studies suggest that dysregulation of the HPA axis activity and disturbance in glucocorticoid receptor (GR) action are involved in the pathogenesis of schizophrenia. The hyperfunction of GR can result from alterations in GR phosphorylation status or numbers of its cochaperones. The most important GR cochaperone FKBP-51, is known to inhibit GR transcriptional activity. The aim of the present work was to investigate the concentration of the immunophilin FKBP-51 in the hippocampus and frontal cortex in a neurodevelopmental animal model of schizophrenia. This model is based on administration of lipopolysaccharide to pregnant rats (in the second and third week of pregnancy). Amount of FKBP-51 was measured by Western blot method. In order to verify the above model, exploration, effi cacy of sensorimotor gating and performance in the social interaction test were determined. Prenatal LPS treatment induced behavioral disturbances typical of schizophrenia, like sensorimotor gating defi cit, higher exploratory activity and changes in social interaction test in the adult offspring. Furthermore, the level of the immunophilin FKBP51 was lower in both female and male offspring. These results suggest that multiple administrations of LPS to pregnant rats evoke GR hyperfunction in adult offspring by decreasing the concentration of FKBP-51, a protein which is known to inhibit GR function. This study was partially supported by the grant N40101231/0174 from the MSHE, Warsaw, Poland.
16

The effect of antidepressant drugs on immunoendocrine changes in animal models of depression

39%
Budziszewska B., Kubera M., Szymanska M., Basta-Kaim A., Grygier B., Lason W.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Exacerbated glucocorticoids and cytokines action are essential factor in the pathogenesis of depression, and the effects of antidepressant drugs on these parameters are poorly recognized.We investigated the effect of antidepressant drugs on the HPA axis activity in prenatally stressed S-D rats and on cell-mediated immunity in Wistar rats and C57BL/6 mice subjected to chronic mild stress (CMS) model of depression. The activity of HPA axis was estimated by measuring the level of glucocorticoid receptors (GR) and activity of some kinases which are known to infl uence GR action. Adult rats subjected to prenatal stress displayed prolonged immobility in the Porsolt test and in open-fi eld test, elevated corticosterone level, increased GR level in the hippocampus but not in frontal cortex. They also showed decreased FKBP51 in the frontal cortex, but not in hippocampus, decreased the active, phosphorylated form of the JNK1 and 2 kinase in the hippocampus and the active form of p38-MAPK in the frontal cortex. Chronic imipramine, fl uoxetine, mirtazapine or tianeptine administration normalized most of these parameters. In CMS model of depression anti-anhedonic effect of imipramine was accompanied by decreased proliferative activity of splenocytes and their ability to produce pro-infl ammatory cytokines in rats. In desipramine treated mice subjected to CMS increased ability of T cells to produce negative immunoregulator IL-10 and decreased the cytotoxic activity of NK cells were observed.
17

Inhibitory effect of neurosteroids on gluicocorticoid receptor-mediated gene transcription:an involvement of protein kinases and interaction with psychotropie drugs

39%
Leskiewicz M., Basta-Kaim A., Budziszewska B., Tetich M., Otczyk M., Lason W.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
18
Content available remote

Inhibitory effect of antipsychotic drugs on the CON A- and LPS- induced proliferative activity of mouse splenocytes: a possible mechanism of action

39%
Basta-Kaim A., Budziszewska B., Jagla G., Nowak W., Kubera M., Lason W.
Journal of Physiology and Pharmacology
|
2006
|
tom 57
|
nr 2
Antipsychotic drugs are widely used to alleviate a number of psychic disorders and have been found to modulate some immune parameters, but the molecular mechanism of their action on the proliferative activity has been poorly recognized. In the present study, we investigated effects of various antipsychotics on the proliferative activity of lymphocytes stimulated by concanavalin A (Con A) and lipopolysaccharide (LPS). Chlorpromazine (3x10-6 - 10-4M) showed the most potent effect in inhibiting 3H-thymidine incorporation into C57BL/6 mouse spleen cells stimulated by Con A and LPS. Treatment of the cells with thioridazine (10-5 - 10-4M), promazine (10-5 - 10-4M), haloperidol (10-5 - 10-4M), risperidone (10-5 - 10-4M), raclopride (3x10-5 - 10-4M), remoxipride (3x10-5 - 10-4M) and clozapine ( 3x10-5 - 10-4M), but not with sulpiride (10-7 - 10-4M), suppressed proliferative activity of splenocytes after Con A stimulation. On the other hand, LPS-induced proliferation of splenocytes was inhibited by clozapine, promazine, thioridazine and haloperidol, but not by risperidone, remoxipride, sulpiride and raclopride. In the next part of the study, the influence of some kinase modulators on chlorpromazine- and clozapine-evoked inhibition of the proliferative activity of splenocytes was determined. Wortmannin, a selective phosphatidylinositol 3-kinase (PI3-K) inhibitor, blocked chlorpromazine and clozapine inhibitory effect on the mitogen-stimulated splenocyte proliferation. The involvement of PI 3-K /protein kinase B (PKB, Akt) pathway was confirmed by the results of the Western blot study, which showed that both drugs increased the level of active phospho-Ser-473 Akt, without changing the total Akt level, and decreased the level of active, nonphosphorylated glycogen synthase kinase-3 (GSK-3ß). Additionally, we have found that chlorpromazine action was also attenuated by a selective p-38-MAPK inhibitor, while clozapine effect was suppressed by a protein kinase C (PKC) activator. The obtained results indicated that atypical antipsychotic drugs markedly inhibited the proliferative activity of splenocytes only after ConA stimulation. Inhibition of the proliferative capability of splenocytes by chlorpromazine and clozapine resulted mainly from the activation of PI3-K/Akt pathway.
19
Content available remote

Effects of combined treatment with imipramine and metyrapone on the immobility time, the activity of hypothalamo-pituitary-adrenocortical axis and immunological parameters in the forced swimming test in the rat

39%
Rogoz Z., Budziszewska B., Kubera M., Basta-Kaim A., Jaworska-Feil L., Skuza G., Lason W.
Journal of Physiology and Pharmacology
|
2005
|
tom 56
|
nr 1
Major depression is frequently associated with the hyperactivity of the hypothalamic-pituitary-adrenocortical axis, and glucocorticoid synthesis inhibitors have been shown to exert antidepressant action. The aim of the present study was to examine the effect of joint administration of metyrapone (50 mg/kg) and imipramine (5 and/or 10 mg/kg) on immobility time, plasma corticosterone concentration, the weight of spleens and thymuses and the proliferative activity of splenocytes in rats subjected to the forced swimming test - an animal model of depression. Metyrapone alone (50 mg/kg) reduced the immobility time of rats in the forced swimming test and decreased plasma corticosterone level, but did not change immunological parameters. Joint administration of metyrapone and imipramine (5 and 10 mg/kg) produced a more pronounced antidepressant-like effect than either of the drugs given alone. The forced swimming procedure significantly increased the proliferative activity of splenocytes, that parameter being reduced only by co-administration of metyrapone and imipramine. Joint administration of metyrapone and imipramine inhibited to a similar extend the corticosterone level as did treatment with metyrapone alone (about twofold); however, the plasma corticosterone level in animals treated with metyrapone and the higher dose of imipramine did not differ from the concentration of this steroid in control, not-stressed rats. The obtained results indicate that metyrapone potentiates the antidepressant-like activity of imipramine and exerts a beneficial effect on the stress-induced increase in plasma corticosterone concentration and the proliferative activity of splenocytes. These finding suggest that a combination of metyrapone and an antidepressant drug may be useful for the treatment drug-resistant depression and/or depression associated with a high cortisol level.
20

Immunomodulatory effect of antidepressant drugs in animal models of depression

33%
Kubera M., Basta-Kaim A., Budziszewska B., Jaworska-Feil E., Roman A., Leskiewicz M., Telich M., Korzeniak B., Lason W.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
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