نمایش پرونده ساده آیتم

dc.contributor.authorNayebi, AM
dc.contributor.authorSheidaei, H
dc.date.accessioned2018-08-26T08:09:58Z
dc.date.available2018-08-26T08:09:58Z
dc.date.issued2010
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/50501
dc.description.abstractBackground and the purpose of the study: The available literatures show that 5-HT1A receptors are widely distributed throughout the basal ganglia, and their activation facilitate dopamine release. Neuroleptic drugs such as haloperidol induce Parkinson-like syndrome through blocking brain D-2 receptors. This study aimed to investigate effect of buspirone, a partial agonist of 5HT(1A) receptor, on motor dysfunctions induced by haloperidol and involvement of 5HT(1A) receptors in this regard. Methods: Study was performed on the male mice weighing 25-30 g. Animals were divided randomly to groups of 10 animals. Motor dysfunction was induced by intraperitoneal (i.p.) injection of haloperidol (1 mg/kg). Catalepsy was assayed by bar-test method 5, 60, 120 and 180 minutes after drug administration and motor imbalance was studied by rotarod test. Results and major conclusion: Results showed that buspirone (20 mg/kg, i.p.) decreased significantly haloperidol-induced catalepsy and balance disorder in a dose dependent manner. Furthermore, 8-OH-DPAT (10 mg/kg, i.p.), as an agonist of 5-HT1A receptor, decreased haloperidol-induced catalepsy and balance disorder. The effect of buspirone (20 mg/kg, i.p.) on haloperidol-induced motor disorders was abolished by NAN-190 (10 mg/kg, i.p.), as a 5-HT1A receptor antagonist. From the results it may be concluded that buspirone improves haloperidol-induced catalepsy and balance disorder through activation of 5-HT1A receptors.
dc.language.isoEnglish
dc.relation.ispartofDARU-JOURNAL OF PHARMACEUTICAL SCIENCES
dc.subjectBuspirone
dc.subjectMotor dysfunction
dc.subjectHaloperidol
dc.subject5-HT1A receptors
dc.titleBuspirone improves haloperidol-induced Parkinson disease in mice through 5-HT1A receptors
dc.typeArticle
dc.citation.volume18
dc.citation.issue1
dc.citation.spage41
dc.citation.epage45
dc.citation.indexWeb of science
dc.citation.URLhttp://daru.tums.ac.ir/index.php/daru/article/view/492


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