Effect of Dexamethasone on Striatal Neurotransmissions in the Rats Subjected to Parkinson’s Disease Animal Model
نویسندگان
1 Department of Medicinal Chemistry, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
2 R and D and QC consultant & Hepatitis and AIDS Department, Research and Production Complex, Pasteur Institute of Iran, Tehran, Iran
3 Department of Physiology and Physiology Research Center, Jundishapour University of Medical Sciences, Ahvaz, Iran
4 R and D and QC consultant & Hepatitis and AIDS Department, Research and Production Complex, Pasteur Institute of Iran, Tehran, Iran
5 R and D and QC consultant & Hepatitis and AIDS Department, Research and Production Complex, Pasteur Institute of Iran, Tehran, Iran
6 Department of Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran
7 Department of Medicinal Chemistry, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
doi
10.22038/ijbms.2011.4972چکیده
Objective(s) The aim of this study was to evaluate the effects of dexamethasone on striatal dopaminergic, glutamatergic and gamma amino butyric acid (GABA) ergic neurotransmission in normal and parkinsonian rats. Materials and Methods Dexamethasone (0.15, 0.30, 0.60 and 0.8 mg/kg) was administered to normal or parkinsonian rats (i.p.) followed by the analysis of the striatal neurotransmitters concentrations. Additionally, the effect of dexamethasone on the damaged Substantia nigra pars compata (SNc) neurons has been investigated. Results Dexamethasone resulted in decreased level of striatum glutamatergic-GABAergic and enhanced dopaminergic neurotransmission in normal and parkinsonian rats. In addition, acute treatment with dexamethasone did not improve the lesion at all. Conclusion These findings suggest the new therapeutic mechanism of action for dexamethasone in Parkinson’s disease animal model.
