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Search Results: 1 - 3 of 3 matches for " Marsida Kallupi "
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MT-7716, a novel selective nonpeptidergic NOP receptor agonist, effectively blocks ethanol-induced increase in GABAergic transmission in the rat central amygdala
Marsida Kallupi,Christopher S. Oleata,Koji Teshima,Roberto Ciccocioppo,Marisa Roberto
Frontiers in Integrative Neuroscience , 2014, DOI: 10.3389/fnint.2014.00018
Abstract: The GABAergic system in the central amygdala (CeA) plays a major role in ethanol dependence and the anxiogenic-like response to ethanol withdrawal. A large body of evidence shows that Nociceptin/Orphanin FQ (N/OFQ) regulates ethanol intake and anxiety-like behavior. In the rat, ethanol significantly augments CeA GABA release, whereas N/OFQ diminishes it. Using electrophysiological techniques in an in vitro slice preparation, in this study we investigated the effects of a nonpeptidergic NOP receptor agonist, MT-7716 [(R)-2-3-[1-(Acenaphthen-1-yl)piperidin-4-yl]-2-oxo-2,3-dihydro-1H-benzimidazol-1-yl-N-methylacetamide hydrochloride hydrate], and its interaction with ethanol on GABAergic transmission in CeA slices of na?ve rats. We found that MT-7716 dose-dependently (100–1000 nM) diminished evoked GABAA receptor-mediated inhibitory postsynaptic potentials (IPSPs) and increased paired-pulse facilitation (PPF) ratio of these evoked IPSPs, suggesting a presynaptic site of action of the MT-7716 by decreasing GABA release at CeA synapses. The presynaptic action of MT-7716 was also supported by the significant decrease in the frequency of miniature inhibitory postsynaptic currents (mIPSCs) induced by the nociceptin receptor (NOP) agonist. Interestingly, MT-7716 prevented the ethanol-induced augmentation of evoked IPSPs. A putative selective NOP antagonist, [Nphe1]Nociceptin(1–13)NH2, totally prevented the MT-7716-induced inhibition of IPSP amplitudes indicating that MT-7716 exerts its effect through NOPs. These data provide support for an interaction between the nociceptin and GABAergic systems in the CeA and for the anti-alcohol properties of the NOP activation. The development of a synthetic nonpeptidergic NOP receptor agonist such as MT-7716 may represent a useful therapeutic target for alcoholism.
Endocannabinoid Regulation of Acute and Protracted Nicotine Withdrawal: Effect of FAAH Inhibition
Andrea Cippitelli, Giuseppe Astarita, Andrea Duranti, Giovanni Caprioli, Massimo Ubaldi, Serena Stopponi, Marsida Kallupi, Gianni Sagratini, Fernando Rodrìguez de Fonseca, Daniele Piomelli, Roberto Ciccocioppo
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0028142
Abstract: Evidence shows that the endocannabinoid system modulates the addictive properties of nicotine. In the present study, we hypothesized that spontaneous withdrawal resulting from removal of chronically implanted transdermal nicotine patches is regulated by the endocannabinoid system. A 7-day nicotine dependence procedure (5.2 mg/rat/day) elicited occurrence of reliable nicotine abstinence symptoms in Wistar rats. Somatic and affective withdrawal signs were observed at 16 and 34 hours following removal of nicotine patches, respectively. Further behavioral manifestations including decrease in locomotor activity and increased weight gain also occurred during withdrawal. Expression of spontaneous nicotine withdrawal was accompanied by fluctuation in levels of the endocannabinoid anandamide (AEA) in several brain structures including the amygdala, the hippocampus, the hypothalamus and the prefrontal cortex. Conversely, levels of 2-arachidonoyl-sn-glycerol were not significantly altered. Pharmacological inhibition of fatty acid amide hydrolase (FAAH), the enzyme responsible for the intracellular degradation of AEA, by URB597 (0.1 and 0.3 mg/kg, i.p.), reduced withdrawal-induced anxiety as assessed by the elevated plus maze test and the shock-probe defensive burying paradigm, but did not prevent the occurrence of somatic signs. Together, the results indicate that pharmacological strategies aimed at enhancing endocannabinoid signaling may offer therapeutic advantages to treat the negative affective state produced by nicotine withdrawal, which is critical for the maintenance of tobacco use.
POLITICAL TRANSITION, CORRUPTION IN NEW DEMOCRACIES. SPECIAL CASE ALBANI
Marsida Ashiku , Head of Finance Department
International Journal of Economics and Research , 2011,
Abstract: This paper examines the effect of democratization on income inequality in new democracies country, using data from the World Income Inequality database. We attempt to explain why income inequality rises at much faster in developing nations than in developed ones. Briefly summarized, high and rising corruption increases income inequality and poverty by reducing economic growth ; increase elite political polarization, induce political instability and even threaten the survival of democracy. The paper argue that the key to solving this puzzle lies in a better understanding of the patterns of democratization and the consequences of corruption in new democracies. While democratization ideally takes place after the construction of a solid institutional foundation of rule of law, realistically most developing countries democratize by introducing elections before they have structured a system of accountability. This type of electoral democracy , despite of legitimizing the government, does not hold the ruling elites accountable through an effective system of checks and balances. As a result, corruption becomes rampant at every level. Most importantly, the emergent corruption attenuates the social demands for redistribution during democratization , since corruption leads to tax evasion particularly among the rich and well connected. This evasion in turn reduces tax progressiveness and offsets the welfare implications of the tax system. Additionally , corruption misallocates social welfare and education program spending by redirecting that spending from those who are truly in need to those who are inside the patronage network. In short , corruption enriches a small part of population at the cost of whole society and therefore leads to greater income inequality.
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