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1

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

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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.
2

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

100%
Listos J., Lupina M., Talarek S., Mazur A., Kotlinska J.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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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.
3

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

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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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