Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: LEŚKIEWICZ
Liczba odnalezionych rekordów: 3



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Tytuł oryginału: Chlorpromazine inhibits the glucocorticoid receptor-mediated gene transcription in a calcium-dependent manner.
Autorzy: Basta-Kaim A., Budziszewska B., Jaworska-Feil L., Tetich M., Leśkiewicz M., Kubera M., Lasoń W.
Źródło: Neuropharmacology 2002: 43 (6) s.1035-1043, il., bibliogr. [36] poz.
Sygnatura GBL: 305,141

Hasła klasyfikacyjne GBL:
  • pediatria
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: Antipsychotic drugs can modulate transcription factors ansd also nuclear receptors, but their action on glucocorticoid receptors (GR)-members of the steroid/thyroid hormone receptor family has been studied so far. In the present study we investigated effects of various antipsychotics on the glucocorticol-mediated gene transcription in fibroplast cells, stably tranfected with a mouse mammary tumor virus promoter (LMCAT cells). Chlorpromazine (3-100 ćM) inhibited the corticosterone-induced gene transcription in a concentration- and time-dependent manner. Clozapine showed a similar, but less potent effect, while haloperiod acted only in high concentrations, and other antipsychotics drugs (sulpiride, raclopride, remoxipride) were without any effect. It was also found that a phorbol ester (an activator of protein kinase C (PKC) and A-23187 (Ca2+-ionophore) attenuated the inhibitory effect of chloropromazine on the GR-induced gene transcription. An antagonist of the L-type Ca2+ channel, as an inhibitor of phospholipase C (PLC) inhibited the corticosterone-induced gene transcription, but had no effect on the chlorpromazine-induced changes. The involvement of a PKC/LC pathway in the chlorpromazine action was confirmed by Western blot analysis showed that the drug in question decreased the PLC-á1 protein level, and to a lesser extent that of the PKC-ŕ protein in LMCAT cells. The aferomentioned data suggest that inhibition of the glucorticosteroid-induced gene transcription by chlorpromazine and clozapine may be a mechanism by which these drugs block some effects induced...


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    Tytuł oryginału: Effect of allopregnanolone on D-[3H]-aspartate release and [3H]-glutamate uptake in the hippocampus of kainate-treated mice.
    Autorzy: Leśkiewicz M., Budziszewska B., Jaworska-Feil L., Lasoń W[adysław]
    Źródło: J. Physiol. Pharmacol. 2002: 53 (2) s.243-250, il., tab., bibliogr. 24 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: In order to determine whether the status epilepticus leads to alterations in th e 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 differenses 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 aaacid release from the hippocamp collected 1h after kainate administration. Kainate administration had noeffect on [3H]-glutamate uptake after 1 and 24 h, but elevated that parameter on day 7. Allopregnanolone (10 and 100 ćM) 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]-asparate release from mouse hippocampus during the kainateinduced status epilepticus; moreover, it excludes involvement of this neurosteroid in the regulation of hipocampal [3H]-glutamate uptake in both control and kainate-treated mice.


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    Tytuł oryginału: Effect of antidepressant drugs on the human corticotropin-releasing-hormone gene promoter activity in neuro-2A cells.
    Autorzy: Budziszewska Bogusława, Jaworska-Feil Lucylla, Tetich Małgorzata, Basta-Kaim Agnieszka, Kubera Marta, Leśkiewicz Monika, Lasoń Władysław
    Źródło: Pol. J. Pharmacol. 2002: 54 (6) s.711-716, il., bibliogr. 16 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • genetyka
  • endokrynologia
  • farmacja

    Typ dokumentu:
  • praca doświadczalna
  • komunikat
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: In order to test if antidepressant drugs can directly influence corticotropin-releasing hormone (CRH) gene expression, their effect on CRH gene promoter activity was evaluated in neuro-2A cells stably transfected with a human CRH - chloramphenicol acetyl-transferase plasmid. Forskolin (an activator of adenylate cyclase), but not phorbol 12-myristate 13-acetate (an activator of protein kinase C), ca. 3-fold increased reporter gene activity, which confirms the critical role of the cAMP-responsive element in regulation of the CRH gene. Imipramine and fluoxetine present in the medium for 5 days, in a concentration-dependent manner (3-30 ćM) inhibited the basal acitivity of CRH gene promoter, while tianeptine was inactive. The obtained results indicate that inhibition of the human CHR gene promoter activity by imipramine and fluoxetine, but not tianeptine, may play a role in mechanism by which the former drugs attenuate HPA axis activity.

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