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1

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

100%
Listos J., Talarek S., Fidecka S.
Acta Neurobiologiae Experimentalis
|
2009
|
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.
2

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

100%
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.
3

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

100%
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.
4

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

100%
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.
5

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

100%
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.
6

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

88%
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.
7

Influence of inhibitors of dipeptidyl peptidase-4 (DPP-4) on naloxone-induced morphine withdrawal signs in rats

88%
Listos J., Lupina M., Talarek S., Mazur A., Kotlinska J.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Inhibitors of dipeptidyl peptidase-4 (DPP-4), named as gliptins, are a class of oral antihyperglycemic drugs. They block enzyme – DPP-4, elevating glucagon-like peptide-1 (GLP-1) level. Commonly DPP-4 inhibitors are used to treat diabetes mellitus. An increasing number of data demonstrate that GLP-1 acts as neuropeptide in brain. The exact mechanism of GLP-1 in brain is unclear. It has been demonstrated, that GLP-1 is bound to presynaptic receptors on glutamatergic terminals facilitating glutamate release, without triggering direct postsynaptic effects. GLP-1 is involved in food intake and GLP-1 receptors are located in mesolimbic structures so it is possible that GLP-1 modulators may be involved in addiction. AIM(S): In the present experiment the influence of DPP-4 inhibitor, linagliptin, on morphine withdrawal signs was studied in rats. METHOD(S): Morphine dependence in rats was obtained by administration of increasing doses of morphine, for 8 days. On the 9th day, the subsequent dose of morphine was injected. 1 hour later, naloxone was administered for induction of morphine withdrawal signs in rats. Then, animals were placed into cylinders and number of jumpings was recorded. In order to evaluate the influence of GLP-1 on the expression of morphine withdrawal signs, linagliptin (10 and 20 mg/kg) was administered in rats on the 9th day of the experiment, before the morphine dose. In order to assess the effect of GLP-1 on the acquisition of morphine withdrawal signs, linagliptin (10 and 20 mg/kg) was injected once a day for 8 consecutive days, before morphine injection. RESULTS: In the present study we demonstrated that linagliptin significantly and dose-dependently reduced the expression of morphine withdrawal signs in rats, and only higher dose of linagliptin markedly reduced the acquisition of morphine withdrawal signs in animals. CONCLUSIONS: The present study provides that DPP-4 inhibitor, linagliptin, may be considered as a valuable tool in searching for new strategies in therapy of morphine dependence. FINANCIAL SUPPORT: The study was financed by funds of Medical University of Lublin.
8

Nitric oxide synthase inhibitors protect against the development of sensitization to mephedrone in mice

88%
Talarek S., Listos J., Orzelska-Gorka J., Bielecka G., Kotlińska J.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Mephedrone is a cathinone derivative that possesses powerful psychostimulant and hallucinogenic effects. It is known that mephedrone may act by increasing release and reuptake inhibition of serotonine and dopamine. Mephedrone has a high abuse and health risk liability, with increased tolerance, sensitization, impaired control and a compulsion to use, the predominant reported dependence symptoms. However, the precise mechanisms underlying its psychoactive effects remain unclear. NO is produced from L-arginine by a reaction catalyzed by NO synthase in response to activation of excitatory amino acid receptors. It acts as an endogenous activator of guanylate cyclase and thereby increases the level of an intracellular second messenger, cGMP. NO, a novel neuronal messenger, is involved in a number of physiological and pathophysiological processes. Recent studies indicate that NO may play a role in tolerance, dependence and sensitization to the addictive drugs such as opioids, ethanol, psychostimulants and nicotine. AIM(S): The present studies were undertaken to determine the influence of NO synthase inhibitors: NG‑nitro-L-arginine methyl ester (L-NAME), non-selective NO synthase inhibitor and 7-nitroindazole, selective inhibitor of neuronal NO synthase, in the development of sensitization to locomotor activity following repeated mephedrone administration in mice. METHOD(S): Sensitization to locomotor activity was induced by chronic administration of mephedrone (2.5 mg/kg/day ip, 5 days) in male albino Swiss mice. L-NAME (25, 50 mg/kg) and 7-nitroindazole (10, 20 mg/kg) were injected ip for 5 days, 20 min before mephedrone administration. After a 7-day interval, acute dose of mehedrone (2.5 mg/kg) was injected and locomotor activity was assessed for 30 min. RESULTS: The present experiments demonstrated that coadministration of NO synthase inhibitors: L-NAME and 7-nitroindazole with mephedrone for 5 days protect against the development of mephedrone-induced sensitization to locomotor activity in mice. CONCLUSIONS: The results of the present study suggest that NO may play a role in the development of sensitization to mephedrone in mice. FINANCIAL SUPPORT: The reported study was supported by Founds for Statutory Activity of Medical University of Lublin, Poland.
9

Effects of ethanol, (9)-tetrahydrocannabinol, or their combination on the short-time spatial memory and cognitive flexibility in adolescent and adult male rats in the Barnes maze test

76%
Gibula-Bruzda E., Kedzierska E., Marszalek-Grabska M., Filarowska J., Kotlinska J. H., Talarek S., Listos J.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: During the past few years it has become clear that both ethanol and cannabinoids affect adolescents and adults differently. For example, both Δ9‑tetrahydrocannabinol (THC) and ethanol disrupt spatial learning more potently in adolescents than adults. The fact that both ethanol and THC impair learning and learning-related hippocampal function more potently in adolescents than in adults is obviously of great importance. But, particularly among teens, ethanol and marijuana are often used in combination. Although there have been a number of studies of the combined effects of ethanol and THC, developmental comparisons are conspicuously absent. This is of particular concern given that early misuse of these substances has been linked to an increased likelihood of later substance use and related behavioral problems. AIM(S): The aim of our study was to reveal whether ethanol and/or THC induced greater spatial memory impairment in adolescent than adult male rats using the Barnes maze test when compared to these drugs alone. METHOD(S): Adolescent rats (postnatal day 30) were submitted into four groups, each of them received injection of: 0.9% NaCl, 1.5 g/kg ethanol, 1.0 mg/kg THC or 1.5 g/kg ethanol+1.0 mg/kg THC on 30, 33, 36 and 39 postnatal day. 24 hours after last injection, half of treated animals from each group were tested in the Barnes maze test. The remaining animals were tested at on postnatal day 70. RESULTS: The results show that there was an age effect on spatial memory in Barnes maze test after the ethanol+THC challenge. Specifically, adolescent animals showed more significant deficits in the short‑time spatial memory (probe trial) or cognitive flexibility (reversal learning) than adults. CONCLUSIONS: These novel findings clearly indicate that further understanding of this age–drug interaction is crucial to elucidating the influence that adolescent ethanol+THC use may have on repeated drug use and abuse later in life. FINANCIAL SUPPORT: This work was supported by the Statutory Funds of the Medical University of Lublin (DS 22/16).
10

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

64%
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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