Author/Authors :
Amanlou, Massoud Department of Medicinal Chemistry - Faculty of Pharmacy - Tehran University of Medical Sciences , Siadat, Davar R and D and QC consultant & Hepatitis and AIDS Department - Research and Production Complex - Pasteur Institute of Iran, Tehran , Norouzian, Dariush R and D and QC consultant & Hepatitis and AIDS Department - Research and Production Complex - Pasteur Institute of Iran, Tehran , Aghasadeghi, Mohammad Reza R and D and QC consultant & Hepatitis and AIDS Department - Research and Production Complex - Pasteur Institute of Iran, Tehran , Fathi Moghaddam, Hadi Department of Physiology and Physiology Research Center - Jundishapour University of Medical Sciences, Ahvaz , Piryaei, Mohhamad Department of Genetics - Shahid Beheshti University of Medical Sciences, Tehran , Shafiee Ardestani, Mehdi Department of Physiology and Physiology Research Center - Jundishapour University of Medical Sciences, Ahvaz
Abstract :
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.
Keywords :
Dexamethasone , Dopamine , GABA , Glutamate , Parkinson’s disease
