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Article: Buspirone-induced changes in the serotonergic and non-serotonergic cells in the dorsal raphe nucleus of rats

TitleBuspirone-induced changes in the serotonergic and non-serotonergic cells in the dorsal raphe nucleus of rats
Authors
KeywordsNeuronal nitric oxide synthase (nNOS)
Tyrosine hydroxylase (TH)
Anxiety
Buspirone
Serotonin (5-HT)
Issue Date2010
Citation
Neuroscience Letters, 2010, v. 473, n. 2, p. 136-140 How to Cite?
AbstractBuspirone, a 5-HT (5-hydroxytryptamine, serotonin)1A partial agonist, is being used as an anxiolytic drug. The mechanism of action is explained by an effect on the 5-HT system. The main source of 5-HT in the forebrain is the dorsal raphe nucleus (DRN). However, there are also other populations of non-5-HT neurons in the DRN. Here, we investigated the effect of acute and chronic buspirone treatments on the 5-HT and non-5-HT cells, the neuronal nitric oxide synthase (nNOS) and tyrosine hydroxylase (TH) cells, in the DRN. Rats received either an acute or chronic administration of buspirone or saline. Hereafter, the brains were processed for 5-HT, nNOS, and TH immunohistochemistry. We found that acute and chronic buspirone treatments significantly lowered the mean optical density of nNOS in the DRN as compared to controls. Meanwhile only the chronic buspirone treatment reduced the mean density of 5-HT and TH immunoreactivity but not the acute buspirone as compared to saline treated animals. Our findings suggest that buspirone treatment affects not only the intracellular content of 5-HT but also nNOS and TH. Therefore, the cellular effect of buspirone is more complex than thought. © 2010 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/219859
ISSN
2015 Impact Factor: 2.107
2015 SCImago Journal Rankings: 1.035

 

DC FieldValueLanguage
dc.contributor.authorJahanshahi, Ali-
dc.contributor.authorLim, Lee Wei-
dc.contributor.authorSteinbusch, Harry W M-
dc.contributor.authorVisser-Vandewalle, Veerle-
dc.contributor.authorTemel, Yasin-
dc.date.accessioned2015-09-24T04:44:08Z-
dc.date.available2015-09-24T04:44:08Z-
dc.date.issued2010-
dc.identifier.citationNeuroscience Letters, 2010, v. 473, n. 2, p. 136-140-
dc.identifier.issn0304-3940-
dc.identifier.urihttp://hdl.handle.net/10722/219859-
dc.description.abstractBuspirone, a 5-HT (5-hydroxytryptamine, serotonin)1A partial agonist, is being used as an anxiolytic drug. The mechanism of action is explained by an effect on the 5-HT system. The main source of 5-HT in the forebrain is the dorsal raphe nucleus (DRN). However, there are also other populations of non-5-HT neurons in the DRN. Here, we investigated the effect of acute and chronic buspirone treatments on the 5-HT and non-5-HT cells, the neuronal nitric oxide synthase (nNOS) and tyrosine hydroxylase (TH) cells, in the DRN. Rats received either an acute or chronic administration of buspirone or saline. Hereafter, the brains were processed for 5-HT, nNOS, and TH immunohistochemistry. We found that acute and chronic buspirone treatments significantly lowered the mean optical density of nNOS in the DRN as compared to controls. Meanwhile only the chronic buspirone treatment reduced the mean density of 5-HT and TH immunoreactivity but not the acute buspirone as compared to saline treated animals. Our findings suggest that buspirone treatment affects not only the intracellular content of 5-HT but also nNOS and TH. Therefore, the cellular effect of buspirone is more complex than thought. © 2010 Elsevier Ireland Ltd.-
dc.languageeng-
dc.relation.ispartofNeuroscience Letters-
dc.subjectNeuronal nitric oxide synthase (nNOS)-
dc.subjectTyrosine hydroxylase (TH)-
dc.subjectAnxiety-
dc.subjectBuspirone-
dc.subjectSerotonin (5-HT)-
dc.titleBuspirone-induced changes in the serotonergic and non-serotonergic cells in the dorsal raphe nucleus of rats-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neulet.2010.02.038-
dc.identifier.pmid20178829-
dc.identifier.scopuseid_2-s2.0-77949912214-
dc.identifier.volume473-
dc.identifier.issue2-
dc.identifier.spage136-
dc.identifier.epage140-

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