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<Articles><Article><Journal><PublisherName></PublisherName><JournalTitle>DARU Journal of Pharmaceutical Sciences</JournalTitle><Volume>18</Volume><Issue>1</Issue></Journal><ArticleTitle>Buspirone improves haloperidol-induced Parkinson disease in mice through 5-HT(1A) recaptors.</ArticleTitle><FirstPage>41</FirstPage><LastPage>5</LastPage><AuthorList><Author><FirstName>A</FirstName><LastName>Mohajjel Nayebi A</LastName></Author><Author><FirstName>H</FirstName><LastName>Sheidaei</LastName></Author></AuthorList><History><PubDate PubStatus="received"><Year>2015</Year><Month>11</Month><Day>09</Day></PubDate></History><Abstract>The available literatures show that 5-HT(1A) 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.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 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-HT(1A) 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-HT(1A) receptor antagonist. From the results it may be concluded that buspirone improves haloperidol-induced catalepsy and balance disorder through activation of 5-HT(1A) receptors.</Abstract><web_url>https://daru.tums.ac.ir/index.php/daru/article/view/492</web_url></Article></Articles>
