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1

Seizure-related alterations in the expression of genes coding for excitatory amino acid receptors

100%
Lason W.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
2

Regulation of neuropeptide genes expression in the rat hippocampus

100%
Lason W.
Acta Neurobiologiae Experimentalis
|
1992
|
tom 52
|
nr 3
3

Opioid systems in WAG/Rij rats - a genetic model of absence epilepsy

100%
Lason W.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
4

Obituary

63%
Przegalinski E., Lason W.
Postępy Higieny i Medycyny Doświadczalnej
|
2002
|
tom 56
|
nr 3
251-254
5

Effects of doxorubicin on undifferentiated and retinoic acid (RA)-treated neuroblastoma SH-SYSY cells

63%
Jantas D., Lason W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
6

Oestrogen effects on kainate-induced toxicity in primary cultures of rat cortical neurons

63%
Kajta M., Lason W.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 3
7

Antiapoptotic effects of memantine on staurosporine-induced cell damage in neocortical cultured neurons

51%
Jantas-Skotniczna D., Kajta M., Lason W.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
8

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
9

Interaction of aryl hydrocarbon receptor-mediated apoptosis of neuronal cells with estrogen receptor signaling

51%
Kajta M., Wojtowicz A. K., Mackowiak M., Lason W.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
Aryl hydrocarbon receptor (AhR) may be responsible for dioxin intoxication, which creates severe clinical problems, such as behavioural and cognitive impairments and an increased number of newborns with deformed brains. Thus, activation of AhRs induces neuronal damage, but the mechanism by which this occurs is largely unknown. Because beta-naphthofl avone is an AhR agonist, we evaluated its impact on apoptotic processes in the mouse primary neuronal cell cultures. In order to verify whether AhR-mediated activation of caspase-3 and lactate dehydrogenase (LDH) release were tissue- and age-dependent, we related them to neocortical and hippocampal tissues, both on 1 and 7 days in vitro. In addition to the effects of estrogen receptor (ER) antagonists and selective estrogen receptor modulators (SERMs), the interaction between AhR-induced apoptosis and ER signaling was evaluated by determining the levels and cellular distribution of AhR and ERbeta. beta-naphtofl avone (0.1ñ100 mM) enhanced caspase-3 activity and LDH release in neocortical and hippocampal cells. A high-affi nity ER antagonist, ICI 182,780, and SERM, tamoxifen, enhanced beta-naphtofl avone-mediated apoptosis. Another SERM, raloxifene, and an ERalpha antagonist, methylpiperidino-pyrazole, did not affect beta-naphtofl avone-induced caspase-3 activity. However, they inhibited beta-naphtofl avoneinduced LDH release at late hour post-treatment, thus suggesting delayed control of AhR-mediated neuronal cell death. The apoptotic effects of beta-naphtofl avone were accompanied by increased levels of AhRs, and these receptors colocalized with ERbeta as demonstrated by confocal microscopy. These data provide evidence for direct interaction of the AhR-mediated apoptotic pathway with estrogen receptor signaling, which gives insight into new strategies to treat or prevent AhR-mediated neurotoxicity. This work was supported by the Polish Ministry of Education and Science, grant No. 2P05A 123 30, and also by the Institute of Pharmacology of Polish Academy of Sciences statutory funds.
10

The evaluation of the role of mGluR7 in neuronal apoptotic processes by usage of AMN082, a selective mGluR7 agonist and mGluR7 knockout-derived cells

51%
Jantas D., Lech T., Pilc A., Lason W.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Increasing body of evidence suggests a neuroprotective potential of metabotropic glutamatergic receptor group III (mGluR III) stimulation, however the role of particular subtypes of these receptors (mGluR4, mGluR7, mGluR8) in apoptotic processes is not fully recognized. Of special interest is the study on the role of mGluR7 which is widely expressed throughout the brain and recently developed selective positive allosteric modulator of this receptor, AMN082 (N,N=-dibenzhydrylethane-1,2-diamine dihydrochloride) enables investigation the biological role of mGluR7. In the present study, firstly we evaluated the possible neuroprotective effects of AMN082 (0.001–1 µM) on neurotoxicity induced by various apoptotic [stimuli staurosporine (St), doxorubicin (Dox) and low potassium (LP)] in 7 DIV cerebellar granule cells (CGC). The data showed that AMN082 (0.1–1 µM) partially attenuated the cell death induced by St and LP, but not by Dox. Next, we investigated the role of mGluR7 in neuronal cell death by testing the vulnerability of CGC from wild and mGluR7KO animals to toxic action of St, Dox and LP. No differences between groups under basal conditions have been found. However, after primary deprivation of CGC cells from potassium in culture medium and secondary application of proapoptotic stimuli we observed the higher vulnerability of mGluR7KO CGC to cell damaging effect of St and Dox but not LP. Further experiments performed on cortical glia cells demonstrated higher toxic action of St and Dox in mGluR7KO cells when compared to wild type one. Additionally, in mGluR7KO glia cells we found higher basal and stimulated by St or Dox caspase-3 activity when compared to wild type one. The obtained data suggest that specific stimulation of mGluR7 by AMN082 could be protective against staurosporine and low-potassium induced neuronal ell death. Moreover, the presence of mGluR7 could be particularly important for survival of glia cells under harmful conditions. The study was supported by statutory funds for Institute of Pharmacology PAS and grant No NN405611638 from the Ministry of Science and Higher Education, Warsaw, Poland.
11

Estrogen interaction with apoptotic effects of tetra-chlorodibenzo-p-dioxin in primary neuronal cell cultures

51%
Kajta M., Jantas-Skotniczna D., Lason W.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
12
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.
13

Agonists of mGluRs II/III attenuate the staurosporine-induced toxicity in human neuroblastoma SH-SY5Y cells

51%
Jantas D., Laskiewicz M., Pilc A., Lason W.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Agonists of metabotropic glutamate receptors group II and III (mGluRs II/III) show neuroprotective effects in in vitro and in vivo models of excitotoxicity. However, their influence on neuronal apoptosis remains unknown. In this study the effect of agonists of mGluRs II/III on staurosporine (St)-evoked LDH release was estimated in undifferentiated (UN-) and retinoic acid (RA)-differentiated human neuroblastoma SH-SY5Y cells. It has been found that LY354740 (0.01-100 microM) and ACTP-I (0.01-100 microM), a nonspecific agonists of mGluRs group II and III, respectively when given alone had no effect on cell proliferation and cell viability. However, both of these compounds partially decreased the St-induced cell death in UN- and RA-SHSY5Y. The selective agonist of mGluR7, AMN082 in low concentrations (0.001-1 microM) had no effect on cell proliferation/viability and tended to attenuate the Stinduced toxicity only in UN-SHSY5Y. On the other hand, AMN082 in higher concentrations (>10 microM) had the cell damaging effect in both UN- and RA- SHSY5Y cells. This study indicates that agonists of mGluRs II/III have potential to attenuate cell death evoked by staurosporine - a well recognized inducer of apoptosis. Acknowledgment: The study was supported by grant No NN405611638 from the Ministry of Science and Higher Education, Warsaw, Poland.
14

The influence of LY354740 - an agonist of group-II metabotropic glutamate receptors (mGLuR II) on neuronal apoptosis in primary neurons

51%
Jantas D., Greda A., Pilc A., Lason W.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
A number of studies have shown neuroprotective effects of agonists of group-II metabotropic glutamate receptors (mGluR II) in various experimental models of excitotoxicity. However, an influence of these compounds on neuronal apoptosis is less recognized. We tested the effect of nonspecific agonist of mGluR II, LY354740 ((+)-2-aminobicyclo[3.1.0]hexane-2,6dicarboxylate) on staurosporine and doxorubicin evoked cell death in primary pure neuronal and neuronal-glial cortical cells, as well in cerebellar granule cells (CGC). We found that LY354740 (0.01-10 microM) was protective against staurosporine-evoked cell death in both, pure cortical neurons and CGC with higher efficacy in 12 DIV in comparison with the 7 DIV ones. Moreover, the neuroprotective effect of LY354470 in neuronal-glial cells did not differ from that found in pure neurons. The protective effect of mGluR II agonist was not connected with attenuation the St-induced caspase-3 activity and DNA fragmentation, but this agent decreased the St-evoked necrotic cell death as measured by propidium ioide staining. LY354470 had no influence on doxorubicin-evoked cell death, but attenuated the glutamate-mediated neuronal cell damage. Our data suggest that neuroprotective effects of the mGluR II ligand are stimuli- and development-dependent and are rather connected with attenuation of necrotic-, than the apoptotic cell death. The study was supported by grant No NN405611638 from the Ministry of Science and Higher Education, Warsaw, Poland.
15

Impact of raloxifene and 3,3’-diindolylmethane on neuronal cells exposed to hypoxia

51%
Rzemieniec J., Litwa E., Lason W., Kajta M.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
During the neonatal period of life, hypoxia appears as a major risk factor which may result in complex cerebral dysfunctions like cerebral palsy or seizure disabilities. Natural neuroprotection against hypoxia-induced injury in females is considered to be due to the effects of circulating ovarian hormones, which are lost after ovariectomy or reproductive senescence. Although anti-hypoxic effects of estrogen have been documented, its clinical use has certain limitations. Selective estrogen receptor modulators (SERMs) and selective aryl hydrocarbon receptor modulators (SAhRs) may act as receptor agonists or antagonists in a tissue-specific manner, thus representing a novel approach for the treatment or the prevention of various types of neural degeneration and seizures. In this study we evaluated the mechanism of action of raloxifene and 3,3’-diindolylmethane (DIM) in response to hypoxia in mouse embryonic neuronal cells in primary cultures. Raloxifene is known to bind to estrogen receptors with SERM properties, whereas (DIM) exhibits properties of SAhRs. In our study, hypoxic conditions (5% CO2/95% nitrogen) induced caspase-3 activity and lactate dehydrogenase (LDH) release in the hippocampal cell cultures. Raloxifene and DIM inhibited the hypoxia-induced LDH release by 10–51% and 9–61%, respectively. DIM inhibited also the hypoxia-induced caspase-3 activity by 2–18%, but raloxifene did not affect the hypoxia-induced apoptotic parameter. In our model of hypoxia, estrogen receptor alpha (ER alpha) antagonist MPP (0.01 µM) did not reverse raloxifene-mediated neuroprotection. However, a high-affinity estrogen receptor beta (ER beta) antagonist, PHTPP (0.01 μM), and G-protein coupled receptor 30 antagonist (GPR30), G-15 (0.01 µM), enhanced the neuroprotective effects of raloxifene, which point to neurotoxic potential of ER beta and GPR30 activation in hypoxia. Selective antagonist of aryl hydrocarbon receptors (AhR) alpha-naphthoflavone (1 µM) did not influence neuroprotective action of DIM, thus suggesting AhR-independent effect. These data demonstrated strong neuroprotective potential of raloxifene and DIM which may represent novel therapeutic tools for brain exposed to hypoxic insults. This study was supported by the Polish National Center of Science grant No 2011/01/N/NZ3/04786
16

The protective effect of TRH and its analogues on staurosporine-but not doxorubicin-induced apoptosis in primary cortical neurons

51%
Jantas D., Jaworska-Feil L., Lipkowski A. W., Lason W.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
In the present study we investigated the infl uence of thyrotropinreleasing hormone (TRH, pGlu-His-Pro-NH2) and its more stable analogues: CG-3703 (Montirelin), RGH-2202 (L-6-keto-piperidine-2carbonyl-L-leucyl-L-prolinamide) and Z-TRH (Z-pGlutamyl-Histydyl-Proline) on neuronal apoptosis evoked by staurosporine ñ or doxorubicin, agents activating mitochondrial or extracellular (FAS) apoptotic cell death, respectively. We showed that TRH (0.001ñ10 μM) in U-shape concentration dependent way (effective concentrations: 0.01 and 0.1 μM) partially attenuated the staurosporine (0.5 μM) ñ but not doxorubicin (0.5 μM)-evoked cell damage in mouse 7 DIV cortical neurons only when added 24 h before toxin administration. The TRH analogues (MON, RGH, Z-TRH) were also effective in lower concentration (0.001 μM) than TRH in attenuation of the staurosporine-induced LDH release. Moreover, that benefi cial effect of TRH and its analogues was not accompanied with its infl uence on caspase-3 activity, though the attenuation of number of apoptotic cells was observed in Hoechstís staining. Furthermore, we found that neither PI3-K (wortmannin 10 μM, LY294002 1 μM) nor MAPK/ERK1/2 (PD098059 1 uM and U0126 1 μM) inhibitors were able to abolish protection served by TRH and MON. There was no protection observed when peptides were added concomitantly with staurosporine and doxorubicin. The obtained data showed ameliorating effect of pretreatment with low concentrations of TRH and its analogues on neuronal cell death mediated by agent activating mitochondrial pathway of apoptosis. That effect seems to be caspase-3-independent and does not engage the PI3-K/ Akt and MAPK/ERK1/2 cellular prosurvival pathways. Supported by grant No. 2PO5A15530 from the Ministry of Education and Science (Warsaw, Poland)
17

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
18

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
19

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
20
Content available remote

Effects of estrone on quisqualate-induced toxicity in primary cultures of rat cortical neurons

51%
Kajta M., Marszal M., Kubera M., Lason W.
Journal of Physiology and Pharmacology
|
2005
|
tom 56
|
nr 2
Estrogens exert protective effects against neurotoxic changes induced by over-activation of ionotrophic glutamate receptors, whereas little is known about their interaction with changes mediated by metabotropic glutamate receptors. We evaluated effects of estrone on quisqualate (QA)-induced toxicity in neuronal cell cultures on 7 and 12 day in vitro (DIV). Twenty four hour exposure to QA (150 µM and 300 µM) significantly decreased cell survival in 7 day old cultures, but the 12 day old cultures were more resistant to its toxicity. DNQX (10 µM), an AMPA/kainate receptor antagonist, partly attenuated the toxic effects of QA, whereas LY 367 385 (100 µM), a selective mGluR1alpha antagonist, completely reversed the above effect. QA did not activate, but suppressed spontaneous caspase-3-like activity. Estrone (100 nM and 500 nM) attenuated QA-mediated neurotoxic effects independently of estrogen receptors, as indicated with ICI 182, 780 and without affecting the caspase-3-like activity. At early stage of development in vitro (7 DIV) toxic effects of QA were more profound and mediated mainly by metabotropic glutamate receptors of group I, whereas later (12 DIV) they were mediated mostly by ionotropic AMPA/kainate receptors. The toxic effects of QA were partly accompanied by anti-apoptotic action against spontaneous caspase-3-like activity, possibly due to modulation of neuronal plasticity.
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