Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

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Liczba odnalezionych rekordów: 18



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1/18

Tytuł oryginału: Nitric oxide and convulsions in 4-aminopyridine-treated mice.
Autorzy: Tutka Piotr, Młynarczyk Małgorzata, Żółkowska Dorota, Kleinrok Zdzisław, Wielosz Marian, Czuczwar Stanisław J.
Źródło: Eur. J. Pharmacol. 2002: 437 (1/2) s.47-53, il., tab., bibliogr. s. 52-53
Sygnatura GBL: 312,088

Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

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

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: We studied whether N**G-nitro-L-arginine (NNA), an inhibitor of nitric oxide (NO) synthase as well as L-arginine and molsidomine, two agents elevating NO, influenced convulsions caused by 4-aminopyridine, a K+ channel blocker in mice. NNA, in a dose known to decrease level of NO (40 mg kg -**1), enhanced the susceptibility to intraperitoneal (i.p.) and intracerebroventricular (i,c,v,) 4-aminopyride. L-arginine (500 mg kg -**1) and molsidomine (20 mg kg -**1) alone did not influence 4-aminopyridine-induced seizure activity. Surprisingly, the proconvulsant effect of NNA upon clonic and tonic seizures was potentiated by molsidomine (20 mg kg -**1). No influence of L-arginine on the proconvulsant effect of NNA was found. Taking into account the proconvulsant effect of NNA, an involvement of NO-mediated events in the mechanism of convulsive activity of 4-aminopyridine might by postulated, However, the ineffectiveness of L-arginine and molsidomine to suppress the convulsive activity of 4-aminopyridine as well as a paradoxical potentiation of the proconvulsant effect of NNA by molsidomine seem to exclude the impact of NO pathway on 4-aminopyridine-induced convulsions in mice. Our data suggest that the proconvulsant effect of NNA in this seizure model is caused by other, not related to NO, mechanisms.

    2/18

    Tytuł oryginału: 2- Chloroadenosine, a preferential agonist of adenosine A1 receptors, enhances the anticonvulsant activity of carbamazepine and clonazepam in mice.
    Autorzy: Borowicz Kinga K., Łuszczki Jarogniew, Czuczwar Stanisław J.
    Źródło: Eur. Neuropsychopharmacol. 2002: 12 (2) s.173-179, il., tab., bibliogr. [28] poz.
    Sygnatura GBL: 313,361

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

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

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: 2-Chloroadenosine (0.25 - 1 mg/kg) significantly raised the threshold for electroconvulsions in mice. This preferential adenosine A1 receptor agonist (at 0.125 mg/kg) significantly potentiated the protective activity of carbamazepine against maximal electroshock-induced seizures in mice. 2-Chloroadenosine (1 mg/kg) showed also anticonvulsive efficacy against pentylenetetrazol-evoked seizures, raising the CD50 vale for pentylenetetrazol from 77.2 to 93.7 mg/kg. The drug (at 0.5 mg/kg) significantly enhanced the protective action of clonazepam in this test, decreasing its ED50 value from 0.033 to 0.011 mg/kg. Moreover, aminophylline, a non-selective adenosine receptor antagonist (5 mg/kg), and 8-cyclopentyl-1,3-dimethylxanthine (8-CPX), a selective A1, adenosine receptor antagonist (5 mg/kg) reversed the 2-chloroadenosine (0.125 mg/kg)-induced enhancement of the protective activity of carbamazepine and clonazepam. 2-Chloroadenosine administered alone or combined with antiepileptic drugs, caused neither motor nor long-term memory impairment. Finally, the adenosine A1 agonist did not change the free plasma concentration of antiepileptic, so a pharmacokinetic factor is not probable. Summing up, 2-chloroadenosine potentiated the protective activity of both carbamazepine and clonazepam, which seems to be associated with the enhancement of purinergic transmission mediated through adenosine A1 receptors.

    3/18

    Tytuł oryginału: Propranolol and metoprolol enhance the anticonvulsant action of valproate and diazepam against maximal electroshock.
    Autorzy: Luchowska Elżbieta, Luchowski Piotr, Wielosz Marian, Kleinrok Zdzisław, Czuczwar Stanisław J., Urbańska Ewa M.
    Źródło: Pharmacol. Biochem. Behav. 2002: 71 (1/2) s.223-231, il., tab., bibliogr. [40] poz.
    Sygnatura GBL: 312,498

    Hasła klasyfikacyjne GBL:
  • farmacja

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

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: The anticoconvulsive potential of classical antiepileptics co-administered with á-adrenergic receptor antagonists against generalized tonic-clonic seizures was evaluated in the model of maximal electroshock (MES)-induced convulsions. Propranolol, acebutolol, metoprolol and atenolol were tested in the doses not affecting the electroconvulsive threshold. Propranolol and metoprolol lowered the ED50 of valproate and diazepam. Acebutolol reduced valproate's but not diazepam's ED50 value. In contrast, hydrophilic atenolol, not penetrating via blood-brain barrier, affected neither the action of valproate nor diazepam. None of the studied drugs changed the protective activity of carbamazepine and phenytoin against MES. á-blokers per se did not alter the motor performance of mice. Moreover, propranolol and metoprolol did not influence diazepam-evoked impairment of locomotor activity. The free plasma and brain levels of antiepileptic drugs were not affected by á-blokers. In conclusion, the use of certain á-adrenoceptor antagonists, such as propranolol and metroprolol, might improve the antiepileptic potential of valproate and diazepam.

    4/18

    Tytuł oryginału: Niguldipine impairs the protective activity of carbamazepine and phenobarbital in amygdala-kindled seizures in rats.
    Autorzy: Borowicz Kinga K., Kleinrok Zdzisław, Czuczwar Stanisław J.
    Źródło: Eur. Neuropsychopharmacol. 2002: 12 (3) s.225-233, il., tab., bibliogr. s. 232-233
    Sygnatura GBL: 313,361

    Hasła klasyfikacyjne GBL:
  • farmacja

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

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: There is evidence that some calcium (Ca2+) channel inhibitors enhance the protective activity of antiepileptic drugs. Since clinical trials have not provided consistent data on this issue, the objective of this study was to evaluate the interaction of a dihydropyridine, niguldipine, with conventional antiepileptics in amygdala-kindled rats. Niguldipine (at 7.5 but not at 5 mg/kg) displayed a significant anticonvulsant effect, as regards seizure and afterdisharge durations in amygdala-kindled convulsions in rats, a model of complex partial seizures. No protective effect was observed when niguldipine (5 mg/kg) was combined with antiepileptics at subeffective doses, i.e. valproate (75 mg/kg), diphenylhydantoin (40 mg/kg), or clonazepam (0.003 mg/kg). Unexpectedly, the combined treatment of niguldipine (5 mg/kg) with carbamazepine (20 mg/kg) or phenobarbital (20 mg/kg) resulted in a proconvulsive action. BAY k-8644 (an L-type Ca2+ channel activator) did not modify the protective activity of niguldipine (7.5 mg/kg) or the opposite action of this dihydropyridine (5 mg/kg) in combinations with carbamazepine or phenobarbital. A pharmacokinetic interaction is not probable since niguldipine did not affect the free plasma levels of the antiepileptics. These data indicate that the opposite actions of niguldipine alone or combined with carbamazepine (or phenobarbital) were not associated with Ca2+ channel blockade. The present results may argue against the use of niguldipine as an adjuvant antiepileptic or for cardiovascular reasons in patients with complex partial seizures.

    5/18

    Tytuł oryginału: Effects of tamoxifen, mifepristone and cyproterone on the electroconvulsive threshold and pentetrazole-induced convulsions in mice.
    Autorzy: Borowicz Kinga K., Łuszczki Jarogniew, Matuszek Mariusz, Kleinrok Zdzisław, Czuczwar Stanisław J.
    Źródło: Pol. J. Pharmacol. 2002: 54 (2) s.103-109, tab., bibliogr. 40 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: The aim of this study was to evaluate the efficacy of three antihormones, tamoxifen (TXF, an antiestrogen), mifepristone (MIF, an antiprogesterone) and cyproterone (CYP, an antiandrogen) in two major models of experimental epilepsy, electriccally and pentetrazole (PTZ)-evoked seizures in mice. TXF (20-50 mg/kg) significantly raised the threshold for electroconvulsions in female mice, whereas CYP was active in male mice. Similar effects were observed in castrated mice. Different data were obtained in sexually immature animals since both TXF and CYP exerted anticonvulsive effects in animals of both genders. MIF (5-50 mg/kg) remained without effect on electrically evoked seizures in mice. The anticonvulsive action of TXF was reversed by aminophylline, bicuculline, kainic acid and N-methyl-D-aspartic acid, but not estradiol or strychnine. The protective action of CYP was reversed by aminophylline and bicuculline, but not by testesterone, kainic acid, N-methyl-D-aspartic acid or strychnice. All three antihormones were inffective against PTZ-induced convulsions in mice. Our results suggest that the action of TXF and CYP might be indirectly associated with the respective hormonal receptor-mediated events, but the nature of this dependence is unclear and further investigations are needed to elucidate this phenomenon.

    6/18

    Tytuł oryginału: Interaction of the neurosteroid alphaxalone with conventional antiepileptic drugs in different types of experimental seizures.
    Autorzy: Borowicz Kinga K., Zadrożniak Marek, Świąder Mariusz, Kowalska Aneta, Kleinrok Zdzisław, Czuczwar Stanisław J.
    Źródło: Eur. J. Pharmacol. 2002: 449 (1/2) s.85-90, tab., bibliogr. [30] poz.
    Sygnatura GBL: 312,088

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

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

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • szczury

    Streszczenie angielskie: A number of neurosteroids exert antiseizure and/or neuroprotective properties. The aim of this study was to evaluate the effect of the neurosteroid alphalone on the protective action of conventional antiepileptics in four seizure test. Alphaxalone (up to 5 mg/kg) did not exert a signifcant action against amygdala-kindled seizures in rats, or against pentetrazole- or aminophylline-induced convulsion in mice. The neuroactive steroid at the dose of 2.5 mg/kg significantly raised the threshold for electroconvulsions in mice. at 2.5 mg/kg, alpaxalone diminished the protective activity of valproate against maximal electroshock and at 2.5 - 5 mg/kg against pentetrazole-induced seizures in mice. However, alphaxalone (2.5 mg/kg) did not affect the protective activity of carbamazepine, diphenylhydantoin, phenobarbital or clonazepam against maximal electroshock and 5 mg/kg did not affect that of phenobarbital, clonazepan and ethosuximide against pentetrazole-induced convulsions. Insignificant results were also obtained in the case of co-administration of alphaxalone with phenobarbital, valproate, clonazepam and carbamazepine against aminophylline-evoked seizures in mice. Also, in the kindling model of epilepsy, combinations of the neuroactive steroid (2.5 mg/kg) with valproate, carbamazepine, phenobarbital, diphenylhydantoin or clonazepam at their subprotective doses did not result in pro- or anticonvulsant activity. Valproate (284 mg/kg; the dose used in combination with alphaxalone) produced sgnificant memory deficits in mice. Alpxaxalone (2.5 mg/kg), valproate...

    7/18

    Tytuł oryginału: Influence of agents affecting voltage-dependent calcium channels and dantrolene on the anticonvulsant action of the AMPA/kainate receptor antagonist LY 300164 in mice.
    Autorzy: Świąder Mariusz, Borowicz Kinga K., Porębiak Jacek, Kleinrok Zdzisław, Czuczwar Stanisław J.
    Źródło: Eur. Neuropsychopharmacol. 2002: 12 (4) s.311-319, il., tab., bibliogr. s. 317-319
    Sygnatura GBL: 313,361

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

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

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: It was previously documented that calcium (Caý+) channel inhibitors intensified the protective effects of conventional antiepileptics against electroconvulsions in mice. The aim of this study was to evaluate the effects of Caý+ channel inhibitors (nifedipine, nicardipine and fluarizine) on the anticonvulsant action of the new AMPA/kainate receptor antagonist, 7-acetyl-3-94-aminophenyl)-8,9-dihydro-8-methyl-7H--1,3-dioxazolo[4,5-h][2,3]-benzodiazepine (LY 300164), against maximal electroshock (MES)-induced seizures in mice. Dantrolene (an inhibitor of Caý+ release from intracellular stroes) was also included. Nifedipine (30 mg/kg) and flunarizine (15 mg/kg) raised the threshold for electroconvulsions, being ineffective at lower dose. Nicardipine (up to 30 mg/kg) and dantrolene (up to 20 mg/kg) did not affect this parameter. Flunarizine (10 mg/kg), nicardipine (20 mg/kg) and dantrolene (20 mg/kg) potentiated the efficacy of LY 300164 against MES. However, nicardipine (at 20 mg/kg) raised the free plasma concentraion of LY 300164. Nifedipine (30 mg/kg), given even in a dose raising the electroconvulsive threshold, did not significantly alter the protective effect of LY 300164 against MES. Furthermore, the Caý+ channel agonist - BY k-8644 (at mg/kg) did not influence the protection offered by LY 300164 against MES. Finally, this Caý+ channel activator did not affect the enhanced efficacy of LY 300164 by Caý+ channel modulators. The only exception was the combination of LY 300164 with flunarizine. Combined treatment with LY 300164 and dantrolene (20 mg/kg)...

    8/18

    Tytuł oryginału: Molsidomine potentiates the protective activity of GYKI 52466, a non-NMDA antagonist, MK-801, a non-competitive NMDA antagonist, and riluzole against electroconvulsions in mice.
    Autorzy: Tutka Piotr, Olszewski Krzysztof, Woźniak Małgorzata, Kleinrok Zdzisław, Czuczwar Stanisław J., Wielosz Marian
    Źródło: Eur. Neuropsychopharmacol. 2002: 12 (4) s.321-326, tab., bibliogr. [35] poz.
    Sygnatura GBL: 313,361

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

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

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: The influence of molsidomine, a donor of nitric oxide (NO), L-arginine, a substrate for NO synthesis, and NG-nitro-L-arginine (NNA), an inhibitor of NO synthase, on the protective activity of CGP 40116, GYKI 52466, MK-801, and riluzole against electroconvulsions was studied in mice. Molsidomine (100 mg kg-1; i.p.) potentiated the protective activity of GYKI 52466, MK-801, and riluzole but did not influence the protection offered by CGP 40116. In contrast to molsidomine, L-arginine (500 mg kg-1, i.p.) did not impair the protective activity of any anticonvulsant. In a dose of 40 mg kg-1, NNA administered i.p. did not afect the protection offered by any excitatory amino acid antagonists and riluzole. Combinations of molsidomine with either GYKI 52466 or MK-801 as well as riluzole did not cause a memory deficit in the passive avoidance task. However, the combined treatment of molsidomine with these anticonvulsant resulted in a motor impairment quantified by the chimney test. The lack of effect of L-arginine and NNA on the protective activity of excitatory amino acid antagonist suggests that molsidomine-evoked alterations in the protection provided by some excitatory amino acid antagonists against electroconvulsions are independent of the NO pathway.

    9/18

    Tytuł oryginału: SIB 1893 possesses pro- and anticounvulsant activity in the electroshock seizure threshold test in mice.
    Autorzy: Łuszczki Jarogniew, Borowicz Kinga K., Czuczwar Stanisław J.
    Źródło: Pol. J. Pharmacol. 2002: 54 (5) s.517-520, il., bibliogr. 9 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • komunikat
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: SIB 1893, a non-competitive antagonist of group I metabotropic glutamate receptor sutype 5, administered at the doses ranging between 0.5 - 2 mg/kg markedly lowered the electorconvulsive thershold, whereas if applied at the higher dose of 40 mg/kg, it significantly raised the threshold for electroconvulsions in mice, exhibiting both pro- and anticonvulsive properties in this test.

    10/18

    Tytuł oryginału: Electroconvulsions elevate the levels of lipid peroxidation products in mice.
    Autorzy: Rola Radosław, Świąder Mariusz, Czuczwar Stanisław J.
    Źródło: Pol. J. Pharmacol. 2002: 54 (5) s.521-524, il., bibliogr. 14 poz., sum.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • komunikat
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: The objective of this study was to determine whether electroconvulsions lead to excessive lipid peroxidation. The concentrations of the conjugated dienes (CD) and malonyl dialdehyde (MDA) in the homogenates of the brains after seizures induced with 25 mA current (MES) measured immediately after seizures were significantly higher in comparison with the control brains. There were no significant differences between control group and animals treated with multiple MES. Significant rise in CD concentrations was also observed at 1 h following MES. The results indicate that electroconvulsions may lead to the increased formation of lipid peroxidation products.

    11/18

    Tytuł oryginału: Low-affinity kainate receptor-mediated events reduce the protective activity of phenobarbital and diphenylhydantoin against maximal electroshock in mice.
    Autorzy: Borowicz K. K., Zadrożniak M., Czuczwar S[tanisław] J.
    Źródło: Neuropharmacology 2002: 43 (7) s.1082-1086, tab., bibliogr. [28] poz.
    Sygnatura GBL: 305,141

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

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

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: (2S, 2R)-4-Methylglutamic acid (SYM 2081), a potent selective agonist of GluR5 and GluR6 kainate receptor subtypes, applied at the dose of 15.5 mg/kg, equal to its CD16 value (i.e., a dose required to induce convulsions in 16 p.c. of mice), significantly decreased the electroconvulsive threshold from 7.0 to 5.8 mA. When administered at the dose of 11.5 mg/kg, equal to 75 p.c. of its CD16, it markedly attenuated the protective activity of phenobarbital and diphenylhydantoin, but not that valproate, carbamazepine, or diazepam against maximal electroshock-induced seizures in mice. The respective ED50 values were increased from 18.5 to 23.8 mg/kg for phenobarbital, and from 11.7 to 14.7 mg/kg for diphenylhydantoin. Since the free plasma levels of tboth antiepileptic drugs were not influenced by SYM 2081, the pharmacokinetic interaction does not seem to be involved in the observed results. In conclusion, low-affinity kainate receptor-mediated events might be a factor reducing the protective efficacy of some anitepileptic drugs. Furthermore, the activation of GLuR5 and GluR6 kainate receptor subtypes by endogenous glutamate during seizures may be associated with the drug-resistance phenomenon.

    12/18

    Tytuł oryginału: Wpływ leków przeciwpadaczkowych i substancji oddziałujących na różne układy neuroprzekaźnikowe na drgawkotwórcze i toksyczne działanie wybranych środków ochrony rośliny u myszy : praca doktorska
    Autorzy: Tochman-Gawda Anna, Czuczwar Stanisław Jerzy (promot.).; Instytut Medycyny Wsi w Lublinie
    Źródło: 2002, [2], 148 k. : il., tab., bibliogr. 262 poz., streszcz., maszyn.
    Sygnatura GBL: 45/20051

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia
  • toksykologia

    Typ dokumentu:
  • praca doświadczalna
  • praca doktorska

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    13/18

    Tytuł oryginału: Zatrucie benzodiazepinami a czynność ośrodkowego układu nerwowego.
    Autorzy: Nowak Stanisław, Sobieszek Grzegorz, Błaszczyk Barbara, Stelmasiak Zbigniew, Czuczwar Stanisław J.
    Źródło: Nowa Klin. 2002: 9 (7/8) s.714-717, il., bibliogr. 31 poz., sum.
    Sygnatura GBL: 313,015

    Hasła klasyfikacyjne GBL:
  • toksykologia
  • farmacja
  • neurologia

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: Benzodiazepines (BZD) are effective GAVA enhancers and consequently may interact with other centrally depressant drugs and alcohol. BZD overdose combined with the above agents may be even fatal. Recently, experiemntal data clearly indicate that peripherally administered BZD produce massive apoptosis in brains of infant rodents. Intensive investigations should follow to find out whether this effect can be also extended to clinical conditions.

    14/18

    Tytuł oryginału: Neuroprotekcja w neurologii.
    Autorzy: Stelmasiak Zbigniew, Krzyżanowski Maciej, Nowak Stanisław, Błaszczyk Barbara, Czuczwar Stanisław J.
    Źródło: Nowa Klin. 2002: 9 (7/8) s.734-737, bibliogr. 30 poz., sum.
    Sygnatura GBL: 313,015

    Hasła klasyfikacyjne GBL:
  • neurologia
  • farmacja

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: Glutamate and oxidative stress are main factors responsible for neurodegeneration. Experimental data indicate that some antiepileptic drugs, especially tiagabine and topiramate, exert neuroprotective effects. In experimental models of Alzhemer's and Parkinson's diseases, potent neuroprotection was provided by memantine (in both models), inhibitors of acetylcholinesterase, antioxidants (Alzheimer's disease) and especially dopaminergic agonists or A2A adenosine receptor antagonists (Parkinson's disease). Clinical data accentuate the importance of memantine, dopaminergic agonists and riluzole in chronic neurodegeneartive diseases.

    15/18

    Tytuł oryginału: Neuroprotekcja w padaczce.
    Tytuł angielski: Neuroprotection in epilepsy.
    Autorzy: Małek Robert, Trojnar Michał K., Czuczwar Stanisław J.
    Źródło: Aktual. Neurol. 2002: 2 (4) s.337-342, tab., bibliogr. 58 poz., sum.
    Sygnatura GBL: 313,631

    Hasła klasyfikacyjne GBL:
  • neurologia
  • toksykologia
  • farmacja

    Wskaźnik treści:
  • ludzie

    Streszczenie polskie: Istnieje wiele prac eksperymentalnych potwierdzających, że drgawkom towarzyszą zmiany neurodegeneracyjne. Niektóre z nich sugerują, że neurodegeneracja może osłabiać działanie leków przeciwpadaczkowych (LPP). W tym kontekście wydaje się, że neuroprotekcyjne oddziaływanie na ośrodkowy układ nerwowy (OUN) powinno odgrywać kluczową rolę w farmakoterapii padaczki. Wśród wielu potencjalnych leków neuroprotekcyjnych LPP wydają się zajmować szczególną pozycję. Dzięki ich dużej heterogenności oraz różnorodnym mechanizmom działania już teoretycznie wydają się one dobrymi kandydatami na leki neuroprotekcyjne. Z tego powodu w pracy naszej skupiliśmy się na przedstawieniu dowodów na neuroprotekcyjne działanie LPP, opartych na eksperymentalnych modelach neurodegeneracji u zwierząt. Mimo, że nasza wiedza dotycząca działania neuroprotekcyjnego LPP jest wciąż niekompletna, leki te mogą stać się w przyszłości niezwykle cenne w terapii wielu stanów degeneracyjnych OUN. Szczególnie dużą nadzieję należy wiązać z nowymi LPP, jednak by to potwierdzić, potrzebne są dalsze badania zarówno eksperymentalne, jak i kliniczne.

    Streszczenie angielskie: There are many experimental data conforming that seizures are associated with neurodegeneration. Some of them suggest that neurodegeneration may decrease the efficacy of antiepileptic drugs (AEDs). In this context, neuroprotection should play a crucial role in the pharmacotherapy of epilepsy. Among many potential neuroprotectants, AEDs serum to be in a privileged position. Theoretically, due to their heterogeneity and diverse mechanisms of action, this group is a perfect candidate for brain protectors. Hence, in this study we focus on evidence of neuroprotective properties of AEDs, based on animal experimental models of neurodegeneration. Although our knowledge about the neuroprotective properties of AEDs is still incomplete, there is hope that this group may become very advantageous in the therapy of many neurodegenerative conditions. Particularly new AEDs seem to hold promise. This, however, necessitates further studies both experimental and clinical.

    16/18

    Tytuł oryginału: Neuroprotective effects of an antiepileptic drugs.
    Autorzy: Trojnar Michał K., Małek Robert, Chrościńska Magdalena, Nowak Stanisław, Błaszczyk Barbara, Czuczwar Stanisław J.
    Źródło: Pol. J. Pharmacol. 2002: 54 (6) s.557-566, tab., bibliogr. 70 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

    Typ dokumentu:
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • zwierzęta
  • króliki
  • myszy
  • szczury
  • in vitro

    Streszczenie angielskie: Experimental and clinical data indicate that epilepsy and seizures lead to neuronal cell loss and irreversible brain damage. This neurodegeneration results not only in the central nervous system dysfunction but may also be responsible for the decreased efficacy of some antiepileptic drugs (AEDs). The aim of this review was to assemble current literature dat on neuroprotective properties of AEDs. The list of hypothetical neuroprotectants is long and consists of substances which act via different mechanisms. We focus on AEDs since this heterogenous group of pharmaceuticals, as far as mechanisms of their action and mechanisms of neuronal death are concerned should provide protection in addition to antiseizure effect itself. Most studies on neuroprotection are based on animal experimental models of neuronal degeneration. Electrically and pharmacologically evoked seizures as well as different models of ischemia are frequently used. Algtough our knowledge about properties of AEDs is still not complete and discrepancies ocassionally occur, the group seems to be promising in terms of neuroprotection. Some of the drugs, though, turn out to be neutral or even have adverse effects on the central nervous system, especially on immature brain tissue (barbiturates and benzodiazepines). Unfortunatelly, we cannot fully extrapolate animal data to humans, therefore further well designed clinical trials are necessary to determine neuroprotective properties of AEDs in humans. However, there is a hope that AEDs will have potential to severe as neuroprotectants not only in seizures, but...

    17/18

    Tytuł oryginału: Effect of gabapentin on the anticonvulsant activity of antiepileptic drugs against electroconvulsions in mice: an isobolographic analysis.
    Autorzy: Borowicz Kinga K., Świąder Mariusz, Łuszczki Jarogniew, Czuczwar Stanisław J.
    Źródło: Epilepsia 2002: 43 (9) s.956-963, il., tab., bibliogr. 25 poz.
    Sygnatura GBL: 304,834

    Hasła klasyfikacyjne GBL:
  • toksykologia
  • farmacja
  • neurologia

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

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: Purpose: The objective of this study was the isobolographic evaluation of the interactions between the novel antiepileptic drug (AED) gabapentin (GBP) and a number of other AEDs against electroconvulsion-induced convulsion in mice. Methods: Electroconvulsions were produced by means of an alternating current (ear-clip electrodes, 0.2-s stimulus duration, tonic hindlimb extension taken as the end point). Adverse effects were evaluated with the chimney test (motor performance) and passive-avoidance task (long-term memory). Plasma levels of AEDs were measured by immunofluorescence or high-pressure liquid chromatography. Results: GBP (ó50 mg/kg) remained ineffective on the electroconvulsive threshold. According to the isobolographic analysis, GBP appears to act synergistically with carbamazepine, valproate, phenytion, phenobarbital (PB), lamotrigine (LTG), and LY 300164. The pharmacokinetic events may be responsible for the interactions of GBP/PB and GBP/LTG, because only PB and LTG significantly elevated the plasma concentration of this AED. Conversely, GBP did not affect the plasma levels of other AEDs used in this study. No adverse effects, were induced by combinations of GBP with these AEDs. Conclusions: The isobolographic analysis revealed that combinations of GBP with other AEDs generally results in entin-Antiepileptic drugs-Electroshock maximal-Drug interactions-Seizures-Isobolography.

    18/18

    Tytuł oryginału: Influence of several convulsants on the protective activity of a non-competitive AMPA/kainate antagonist, LY 300164, and lamotrigine against maximal electroshock in mice.
    Autorzy: Borowicz K. K., Świąder M., Zgrajka W., Sawulski C., Turski W. A., Czuczwar S[tanisław] J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 2) s.859-869, tab., bibliogr. 32 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • immunologia
  • farmacja
  • pulmonologia
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: Aminophyline (50-100 mg/kg) and strychnine (0.125-0.5 mg/kg) significantly raised the ED50 values of LY 300164 against maximal electroshock in mice, from 4 to 8 mg/kg (aminophylline 100 mg/kg) and from 3.6 to 11.5 mg/kg (strychnine 0.5 mg/kg). Also, aminophylline (25-50 mg/kg) and strychnine (O.125-0.25 mg/kg) increased the ED50 value of lamotrigine in this test, for instance from 5.5 to 8.0 mg/kg (aminophylline 50 mg/kg) and from 5.2 to 8.9 mg/kg (strychnine 0.25 mg/kg). Moreover, the ED50s values of aminophylline and strychnine for the reduction of the anticonvulsant effect of LY 300164 (7 mg/kg, the dose equal to its ED97 value against maximal electroshock) were 79.9 and 0.2 mg/kg, respectively. The respective ED50 values for the inhibition of the antiseizure action of lamotrigine were 40.9 and 0.2 mg/kg. Neither bicuculline nor picrotoxin affected the protective action of LY 300164 or lamotrigine. Strychnine significantly lowered the plasma concertrations of LY 300164 and this my point to a pharmacokinetic mechanism of the observed interaction. Aminophylline did not affect the plasma concentrations of the studied anticonvulsant drugs and strychnine - that of lamotrigine, so a pharmacokinetic interaction does not seem probable. The present results indicate that the potential of aminophylline and strychnine to attenuate the anticonvulsant activity of conventional antiepileptics is extended to LY 300164 and lamotrigine.

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