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Ethanol and benzodiazepines. The influence of CGS 8216 on the ethanol - induced hypothermia and motor incoordination in mice and rats

100%
Fidecka S., Langwinski R.
Journal of Physiology and Pharmacology
|
1995
|
tom 46
|
nr 4
2

Synthesis and pharmacological evaluation of some novel thiourea derivatives incorporating 3-(trifluoromethyl)phenyl moiety

81%
Kedzierska E., Fidecka S., Bielenica A., Struga M.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 3
Despite the great progress in the treatment of pain, depression, anxiety, and other central nervous system (CNS) disorders, the used drugs do not fulfil all expectations. And there is still a need to search for new, more effective therapies as well as need to know the mechanisms of action of existing drugs. The tested compounds are a group of thiourea derivatives with expected potential central activity in the CNS. Numerous thiourea-derived compounds are selective ligands for 5-HT2 receptors family (Forbes et al. 1995) and also exhibit a broad spectrum of biological activities as analgesic, antidepressant, anticonvulsant, antiviral, anti-HIV, antibacterial, and HDL-elevating properties (Struga et al. 2007, Wardakhan et al. 2008, Karakus et al. 2009). Modification of the chemical structure makes it possible to obtain new compounds with pharmacological activity, higher selectivity and fewer adverse effects. Compounds were studied in behavioral tests used to predict a potential influence on the CNS in mice (after their ip or sc administration). The results of the pharmacological studies showed that new compounds exerted substantial impact on the CNS in mice. The most important seems to be their influence on the transmission of serotonin (activity in the head-twitch test, changes in body temperature) as well as antinociceptive effects. These compounds caused no coordination disorders, and do not affect locomotor activity, but slightly decreased the hyperactivity caused by administration of amphetamine. Obtained results indicate the possibility of the involvement of serotonin in the action of the majority of the compounds.
3

Adenosine receptor agonists attenuate the expression of sensitization to morphine induced place preference in rats

81%
Listos J., Talarek S., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2009
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tom 69
|
nr 3
Behavioural sensitization is an enhancement of certain drug-induced effects which develops following repeated, intermittent exposure to opioids and psychoactive drugs. The sensitization can be measured in various animal models, e.g. conditioned place preference paradigm. In the present studies we undertook to investigate an involvement of adenosine receptor agonists in expression of sensitization to morphine-induced rewarding effects in rats. Three, intraperitoneal (i.p.) injections of morphine (5.0 mg/kg) induced conditioned place preference. Five days later, in animals with prior history of morphine administration, ineffective dose of morphine (0.75 mg/kg i.p.) was administered. That dose was able to induce a signifi cant intensifi cation of morphine response in conditioned place preference paradigm. It showed that morphine-induced sensitization to rewarding effects had been developed. To determine the effects of adenosine receptor agonists on expression of sensitization, selective and non-selective drugs were administered 15 min before the last injection of morphine. We showed that all adenosine drugs were able to attenuate the expression of morphine sensitization and the strongest effects were produced by selective (A1) and non-selective (A1 and A2A) adenosine receptor agonists. We conclude that adenosine agonists may play an important role in drugseeking behaviour underlying the development of addiction.
4

The effect of adenosinergic system on development of sensitization to morphine-induced withdrawal signs in rats

81%
Listos J., Talarek S., Orzelska J., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 3
In the presented study the effect of continuous and sporadic treatment with morphine (MPH) on the severity of MPH withdrawal signs was examined in rats. Also, the effect of A1 and A2A adenosine agonists (N6-cyclopentyladenosine and 2-p-(2-carboxyethyl) phenethylamino5’-N- ethylcarboxamidoadenosine hydrochloride, respectively) on development of this sensitization was studied. Rats were treated with increasing doses of MPH and were divided into groups. First group received MPH for 8 consecutive days (continuous group), the second, received MPH in four two-day periods with three 36-hour breaks (sporadic group). Control group received saline. Adenosine drugs were administered during three MPH-free periods (6 injections). Last day, to induce withdrawal signs, 1 hour after MPH injection, naloxon was administered. The number of jumps was recorded for a period of 30 min. Jumps were significantly greater in sporadic group in compare with continuous group, which confirm that sensitization to MPHinduced withdrawal signs has been developed. There were not any jumps in control rats. Rats showed that stimulation of A2A receptors inhibited the withdrawal signs. Less significant effect was observed after stimulation of A1 receptors. The findings showed that repeated withdrawal episodes intensified the severity of withdrawal signs and adenosinergic system, mainly by A2A receptors, was able to inhibit the development sensitization to MPH withdrawal signs.
5

Participation of NO:sGC pathway in the development of tolerance to mephedrone in mice

81%
Talarek S., Lisos J., Orzelska J., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 3
Mephedrone is a cathinone derivative that possesses powerful psychostimulant and hallucinogenic effects. It has been speculated that mephedrone may act by increasing release and reuptake inhibition of serotonine and dopamine. However, the precise mechanisms underlying its psychomimetic action remain unclear. Nitric oxide (NO), synthesized from L-arginine by a reaction catalyzed by NO synthase, is involved in different central function and can participate in the mechanisms of drug tolerance and dependence. NO acts as an activator of soluble guanylyl cyclase (sGC) and thereby increases the level of an intracellular second messenger, cGMP. The purpose of the present study was to determine the role of NO in the development of tolerance to mephedrone. Tolerance to hyperlocomotor activity was induced by chronic administration of mephedrone (5 mg/kg ip, 6 days) in male albino Swiss mice. The following drugs were used to modify the NO:cGMP pathway: NG-nitro-L-arginine methyl ester (L-NAME; 25, 50 mg/kg, ip) – NO synthase inhibitor and methylene blue (5, 10 mg/kg ip) – sGC inhibitor. Locomotor activity was measured for 10 and 30 min, 20 min after administration of drugs. The present experiments demonstrated that chronic coadministration of L-NAME and methylene blue with mephedrone attenuates the development of tolerance to mephedrone. These findings suggest that NO:sGC pathway may be involved in the tolerance to mephedrone in mice.
6

Agmatine inhibits flunitrazepam-induced memory impairment in the mEPM in mice

81%
Orzelska J., Talarek S., Listos J., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 3
Benzodiazepines (BZ) have long been known to impair memory as a result of their action at γ-aminobutyric acid (GABA)A receptors. But it is not clear what stages of memory (acquisition, consolidation or retrieval) are affected by BZ. Flunitrazepam (FNZ) – one of the BZ drug – has highly ability to cause amnesia and it is known as a daterape drug. Recent evidence suggests that agmatine (AGM), the metabolite of L-arginine, exists in the mammalian brain and can modulate behavior function, including learning and memory. The mechanism of AGM action has not been completely explained. Many studies showed that AGM regulates the L-arginine:nitric oxide(NO):cGMP pathway because AGM is a metabolite of L-arginine and AGM can inhibit neuronal NO synthase. Our previous research has indicated that modulators of L-arginine:NO:cGMP affected BZ-induced memory impairment. The aim of this study was to assess the role of AGM in the amnesic effects of FNZ in the modified elevated plus-maze task (mEPM) in mice. Our experiments showed that FNZ (0.05 and 0.1 mg/kg, sc) disrupted acquisition and consolidation of memory in mice. The amnesic properties of FNZ were prevented by AGM (20 mg/kg, ip – the acquisition stage) and (5, 10 and 20 mg/ kg, ip – the consolidation stage). The above results suggest that AGM may be involved in the amnesic effects of FNZ.
7

Ethanol-induced hypothermia, cross tolerance with morphine

81%
Fidecka S., Tamborska E., Langwinski R.
Acta Physiologica Polonica
|
1986
|
tom 37
|
nr 4-5
8

Participation of nitric oxide in TH benzodiazepine withdrawal syndrome in mice and rats

81%
Fidecka S., Lalewicz S., Poleszak E.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
9

The involvement of nutric oxide (NO) in the amnesic effects of diazepam in mice

81%
Talarek S., Orzelska J., Listos J., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Literature data show the relationship between L-arginine:NO:cGMP pathway and g-aminobutyric acid (GABA)-mediated transmission in the central nervous system. Benzodiazepines are known to enhance the GABA-ergic neurotransmission and well established as inhibitory modulators of memory processing. More-over, the role of NO in learning and memory processes has been proposed. The present studies were designed to evaluate the role of L-arginine:NO:cGMP pathway in the amnesic effects of diazepam (DZ) in the modifi ed elevated plus-maze (mEPM) task in mice. Our experiments indicated that DZ (1 mg/kg, s.c.) impaired elevated plus-maze memory performance in mice. Pretreatment with L-arginine, the NO precursor, (500 mg/kg, i.p.) prevented the amnesic properties of DZ. While, 7-nitroindazole (7-NI), the neuronal NO synthase inhibitor (nNOS), (40 mg/kg, i.p.) and methylene blue (MB), the soluble guanylate cyclase (sGC) inhibitor, (5 mg/kg, i.p.) enhanced the DZ-induced memory defi cits. Moreover, the effect of both 7-NI and MB were reversed by L-arginine (250 mg/kg, i.p.). It is important to note that presented data are not due to either 7-NI-, MB-induced impairment of memory or changes in locomotor activity, because 7-NI and MB given alone, had no impact on the mEPM behaviour and locomotor activity of mice. Taken together, these results suggest that an inhibition of the Larginine:NO:cGMP pathway may be involved in the amnesic effects of benzodiazepines.
10

The effect of NMDA receptor antagonists on the development of sensitization to diazepan withdrawal signs in mice

71%
Talarek S., Listos J., Orzelska J., Lupina M., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Repeated administration of benzodiazepines can alter GABAA receptors, which contributes to the development of dependence and often limits their clinical use. Although multiple chemical mediators are now hypothesized to be involved in the addictive effect of benzodiazepines, the mechanisms involved in the benzodiazepine dependence are not fully understood. The aim of the present study was to investigate the effects of two uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists, ketamine and memantine, on the development of sensitization to diazepam withdrawal signs in mice. METHODS: In order to show the sensitization to benzodiazepine withdrawal signs the animals were divided into groups: the animals continuously (for 21 days) treated with diazepam (15 mg/kg/day sc) and the animals receiving diazepam during three 7-day periods interspersed with 3 day diazepam-free period in which the animals were treated with vehicle injections. Ketamine (2.5, 5 mg/kg ip) or memantine (2.5, 5 mg/kg ip) were administrated in sporadic diazepam treated mice during the diazepam-free periods (three, daily injections in each of the periods). In all animals, the intensity of diazepam withdrawal signs, observed as the increase in seizure activity (in pentylenetetrazole (PTZ)-induced seizures model) was assessed 48 h after the last injection of diazepam or vehicle. The animals, after concomitant administration of subthreshold dose of PTZ (55 mg/kg sc) with flumazenil (5 mg/kg ip), were placed in glass cylinders and were observed for 60 min. RESULTS: The present experiments showed that administration of ketamine (2.5, 5 mg/kg) or memantine (2.5, 5 mg/kg) during two diazepam drug-free periods in sensitized mice, significantly attenuated their seizures activity. CONCLUSION: These findings support the hypothesis that glutamatergic system is involved in the mechanisms of sensitization to withdrawal signs precipitated after sporadic treatment with diazepam.
11

Morphine dependence in rats: effect of low-level lead exposure during perinatal period

71%
Listos J., Listos P., Baranowska-Bosiacka I., Chlubek D., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
In the present experiments the effect of perinatal lead exposure on development of morphine dependence in rats was examined. Female rats were gavaged daily with 0.1 % lead acetate solution. Lead ions were administered through pregnancy and two months through lactation. In the same time control animals received water. The development of morphine dependence was obtained by administration of increasing doses (10, 20, 30, 40, 50, 50 mg/kg, ip) of morphine for six consecutive days in lead intoxicated rats and in control animals. 20 min after the last injection of morphine the withdrawal signs were induced by application of naloxon at dose of 2 mg/kg, ip. Secondly, the development of morphine tolerance to antinociception activity was studied in the tail-flick test in lead intoxicated rats. Then rats received morphine (10 mg/kg, ip) for seven consecutive days and test was performed on 1st and 7th day of the experiment. The experiments have shown that in lead intoxicated rats morphine withdrawal signs (jumping, wet dog shakes) were significantly potentiated than in control animals. The morphine tolerance was also more expressed in lead intoxicate rats. The obtained results have shown that prenatal lead exposure intensify the effects of chronic treatment with morphine in rats.
12

NMDA-glutamate mechanism of magnesium-induced anxiolytic-like activity

71%
Poleszak E., Wlaz P., Wrobel A., Fidecka S., Nowak G.
Journal of Elementology
|
2008
|
tom 13
|
nr 3 Suppl.
13

Analysis of possible allosteric modulation of opioid signaling

61%
Bartuzi D., Kaczor A., Kijkowska-Murak U., Fidecka S., Kedzierska E., Matosiuk D.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
Administration of classic orthosteric ligands of opioid receptors, like morphine, apart from inducing significant therapeutic effects such as analgesia, presents many disadvantages, with drug addiction and impairment of the breathing centre on the first place. However, allosteric modulation of these receptors could offer better selectivity among receptor subtypes and preservation of the physiological pattern of activation [1]. All in all, such compounds could bring more advantageous pharmacological profile, and decrease possibility of undesirable side effects. The aim of work was to investigate the mode of interaction of the unique ligands [2-5] with MOR and DOR opioid receptors. As premises of allosteric pockets existence appeared, establishment of a possible mode of interaction between ortho- and allosteric pocket became an consecutive aim. Models of the receptors were obtained with the method of homology modelling, using β2-adrenergic receptor as a template. These models were initially verified by rigid docking of rigid opiod receptors’ ligands (SIOM and naloxone). Best protein models were chosen for flexible dockings. Analysis of the results revealed that investigated compounds could be bound into two different pockets on the extracellular receptor’s surface near the orthosteric pocket. Location of those hypothetical binding sites suggests, that their interaction with ligands could significantly modulate function of the receptor. The hypothetical pocket located between extracellular parts of TM1, TM2 and TM7 seems to share important amino acids with orthosteric pocket. Moreover, the other hypothetical binding site is located in ECL2 region, and seems to be analogous to allosteric binding site discovered in muscarinic M2 receptor structure [6].
14

The influence of magnesium on the action of the anti-depressant drugs in swim test in mice

61%
Poleszak E., Kedzerska E., Wlaz P., Nowak G., Fidecka S., Pilc A.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
15

Sensitization to morphine withdrawal signs-a neurochemical basis in dopaminergic receptors

51%
Listos J., Wasik A., Bosiacka I., Talarek S., Orzelska J., Lupina M., Antkiewicz-Michaluk L., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: In morphine addicted patients, chronic treatment with various abusers is interspersed with drugfree periods (periods of sleep or unsuccessful attempts to treat). These repeated withdrawal periods may intensify the withdrawal episode. These data inspired us to examine if repeated withdrawal periods has the effect on the severity of naloxone-induced withdrawal signs in rats. We also investigated the effect of A1 and A2A receptors in observed withdrawal signs. Additionally, to elucidate the mechanisms underlying the effects of repeated morphine withdrawal signs, neurochemical experiments were performed. METHODS: To obtain the state of dependence, the animals were treated with increasing doses of morphine, twice a day, for 8 days. To demonstrate the effect of sporadic treatment with morphine, we divided rats into two groups: continuously and sporadically treated with morphine. In sporadic group, morphine administration was modified by adding 3 morphine-free periods. On the 9th day of the study, the subsequent dose of morphine was injected. 1 hour later, the naloxone, was administrated for induction of morphine withdrawal signs in rats. Then, animals were placed into cylinders and jumpings were recorded for period 30 min. After decapitation, a neurochemical study, using HPLC-ED method was made. The concentration of dopamine and its metabolites was assessed in three brain structures (striatum, hippocampus, prefrontal cortex). RESULTS: We confirmed that sporadic treatment with morphine induced the intensification of morphine withdrawal signs, and administration of both adenosine agonists reduced the severity of them. In neurochemical experiments we demonstrated significant differences in the release in dopamine and its metabolites in studied brain areas. CONCLUSION: The recognition of neurochemical mechanisms, underlying the behavioral changes, may have an important role for further exploration of the various effects of repeated morphine withdrawal signs.
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