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dc.contributor.authorMatteo, Vincenzo di
dc.contributor.authorPierucci, Massimo
dc.contributor.authorBenigno, Arcangelo
dc.contributor.authorEsposito, Ennio
dc.contributor.authorCrescimanno, Giuseppe
dc.contributor.authorDi Giovanni, Giuseppe
dc.date.accessioned2017-10-13T17:17:41Z
dc.date.available2017-10-13T17:17:41Z
dc.date.issued2010
dc.identifier.citationDi Matteo, V., Pierucci, M., Benigno, A., Crescimanno, G., Esposito, E., & Di Giovanni, G. (2010). Critical role of nitric oxide on nicotine-induced hyperactivation of dopaminergic nigrostriatal system: electrophysiological and neurochemical evidence in rats. CNS Neuroscience & Therapeutics, 16(3), 127-136.en_GB
dc.identifier.urihttps://www.um.edu.mt/library/oar//handle/123456789/22592
dc.description.abstractNicotine, the main psychoactive ingredient in tobacco, stimulates dopamine (DA) function, increasing DA neuronal activity and DA release. DA is involved in both motor control and in the rewarding and reinforcing effects of nicotine; however, the complete understanding of its molecular mechanisms is yet to be attained. Substantial evidence indicates that the reinforcing properties of drugs of abuse, including nicotine, can be affected by the nitric oxide (NO) system, which may act by modulating central dopaminergic function. In this study, using single cell recordings in vivo coupled with microiontophoresis and microdialysis in freely moving animals, the role of NO signaling on the hyperactivation elicited by nicotine of the nigrostriatal system was investigated in rats. Nicotine induced a dose-dependent increase of the firing activity of the substantia nigra pars compacta (SNc) DA neurons and DA and 3,4-dihydroxyphenylacetic acid (DOPAC) release in the striatum. Pharmacological manipulation of the NO system did not produce any change under basal condition in terms of neuronal discharge and DA release. In contrast, pretreatments with two NO synthase (NOS) inhibitors, N-ω-nitro-l-arginine methyl ester (l-NAME) and 7-nitroindazole (7-NI) were both capable of blocking the nicotine-induced increase of SNc DA neuron activity and DA striatal levels. The effects of nicotine in l-NAME and 7-NI-pretreated rats were partially restored when rats were pretreated with the NO donor molsidomine. These results further support the evidence of an important role played by NO on modulation of dopaminergic function and drug addiction, thus revealing new pharmacological possibilities in the treatment of nicotine dependence and other DA dysfunctions.en_GB
dc.language.isoenen_GB
dc.publisherWiley-Blackwell Publishing Ltd.en_GB
dc.rightsinfo:eu-repo/semantics/restrictedAccessen_GB
dc.subjectNitric oxideen_GB
dc.subjectNicotineen_GB
dc.subjectDopamineen_GB
dc.subjectCorpus striatumen_GB
dc.titleCritical role of nitric oxide on nicotine-induced hyperactivation of dopaminergic nigrostriatal system : electrophysiological and neurochemical evidence in ratsen_GB
dc.typearticleen_GB
dc.rights.holderThe copyright of this work belongs to the author(s)/publisher. The rights of this work are as defined by the appropriate Copyright Legislation or as modified by any successive legislation. Users may access this work and can make use of the information contained in accordance with the Copyright Legislation provided that the author must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the prior permission of the copyright holder.en_GB
dc.description.reviewedpeer-revieweden_GB
dc.identifier.doi10.1111/j.1755-5949.2010.00136.x
dc.publication.titleCNS Neuroscience & Therapeuticsen_GB
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