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dc.contributor.authorNayebi, AM
dc.contributor.authorRad, SR
dc.contributor.authorSaberian, M
dc.contributor.authorAzimzadeh, S
dc.contributor.authorSamini, M
dc.date.accessioned2018-08-26T08:12:23Z
dc.date.available2018-08-26T08:12:23Z
dc.date.issued2010
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/50768
dc.description.abstractReceptors for 5-HT1A are widely distributed throughout the basal ganglia, and their activation results in an inhibition of dopamine (DA) release. This study aimed to investigate the effect of buspirone, as a partial agonist of 5-HT1A receptors, on 6-hydroxydopamine (6-OHDA)-induced catalepsy in male Wistar rats. Catalepsy was induced by unilateral infusion of 6-OH-DA (6 mu g/2 2 mu l/rat) into the central region of the substantia nigra pars compacta (SNc) and assayed by the bar-test method 60, 120 and 180 min after drug administration. The results demonstrated that intraperitoneal (ip) injection of buspirone at doses of 5, 7.5 and 10 mg/kg decreased catalepsy compared with the control group. In addition, intra-SNc injection of 8-hydroxy-2-[di-n-propylamino]tetralin (8-OH-DPAT; 10 mu g/rat), a 5-HT1A receptor agonist, decreased 6-OHDA-induced catalepsy. The effects of buspirone (7.5 mg/kg, ip) and 8-OH-DPAT (10 mu g/rat, intra-SNc) were abolished by 1-(2-methoxyphenyl)-4-[4-(2-phthalimido) butyl]piperazine hydrobromide (NAN-190; 10 mu g/rat, intra-SNc), a 5-HT1A receptor antagonist. Our study indicates that buspirone improves catalepsy in a 6-OHDA-induced animal model of Parkinson's disease through activation of nigral 5-HT1A receptors. However, further investigations should be undertaken to clarify the exact mechanism of interaction between 5-HT1A and DA receptors.
dc.language.isoEnglish
dc.relation.ispartofPHARMACOLOGICAL REPORTS
dc.subjectbuspirone
dc.subject5-HT1A receptor
dc.subject6-hydroxydopamine
dc.subjectcatalepsy
dc.subjectrat
dc.titleBuspirone improves 6-hydroxydopamine-induced catalepsy through stimulation of nigral 5-HT1A receptors in rats
dc.typeArticle
dc.citation.volume62
dc.citation.issue2
dc.citation.spage258
dc.citation.epage264
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.1016/S1734-1140(10)70264-4


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