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Buspirone improves haloperidol-induced Parkinson disease in mice through 5-HT1A receptors

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نمایش/بازکردن
DARU-18-041.pdf (349.0Kb)
تاریخ
2010
نویسنده
Nayebi, AM
Sheidaei, H
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نمایش پرونده کامل آیتم
چکیده
Background 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.
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http://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/50501
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