Effects Of Nicotine On GLU And GABA Neurons In Rats With Parkinson's Disease

Objective:Observing the dynamic changes of the expression of glutamate and gamma aminobutyric acid during the development of rotenone sunflower oil emulsion induced Parkinson's disease rats and the intervention effect on it with different doses of nicotine. Methods:Pick 48 healthy female SD rats which weigh 200~250g. Randomly divided them into four groups:control group(n = 12), rotenone group(n = 12), rotenone + nicotine(0.5mg/kg) group(n = 12), rotenone + nicotine(1.0mg/kg) group(n = 12). Control group was injected of normal saline, rotenone group was injected of normal saline and rotenone sunflower oil emulsion liquid(1.5mg/kg), rotenone + nicotine(0.5mg/kg) group was injected of nicotine(0.5mg/kg) and rotenone sunflower oil emulsion liquid(1.5mg/ kg), rotenone + nicotine(1.0mg/kg) group was injected of nicotine(1.0mg/kg) and rotenone sunflower oil emulsion liquid(1.5mg/ kg). Test behaviors of each group rats in 2 weeks, 4 weeks, 6 weeks and 7 weeks, then rats were detected by immunohistochemical method on the expression of rat brain substantia nigra GLU and GABA. Result: 1. Nicotine antagonizes the decrease of locomotor activity function of rats induced by rotenone.Rotenone treated rats in 2 weeks, 4 weeks, 5 weeks, lattice numbers were less than the control group(P < 0.05), however, the lattice numbers of rats that pretreated with different doses of nicotine(0.5, 1.0mg/kg) were increased contrast to the rotenone group(P < 0.05), but there were no differences in two different concentrations of nicotine treatment(P > 0.05). This suggests that nicotine can antagonize the decrease of locomotor activity function of rats induced by rotenone. 2. Nicotine antagonizes the decrease of motor coordination function of rats induced by rotenone.Rotenone treated rats in 2 weeks, 4 weeks, 5 weeks, the angles of inclination were less than the control group(P < 0.05), however, the lattice numbers of rats that pretreated with different doses of nicotine(0.5, 1.0 mg/kg) were increased contrast to the rotenone group(P < 0.05), but there were no differences in two different concentrations of nicotine treatment(P > 0.05). This suggests that nicotine can antagonize the decrease of motor coordination function of rats induced by rotenone. 3. Nicotine antagonizes the increase of expression of rat midbrain substantia nigra GLU immunoreactive positive cells induced by rotenone.Rotenone treated rats in 2 weeks, 4 weeks, 5 weeks, the expression of rat midbrain substantia nigra GLU immunoreactive positive cells were higher than the control group(P < 0.05), however, the expression of GLU in rats that pretreated with different doses of nicotine(0.5, 1.0 mg/kg) were decreased contrast to the rotenone group(P < 0.05), but there were no differences in two different concentrations of nicotine treatment(P > 0.05). This suggests that nicotine can antagonize the increase of expression of rat midbrain substantia nigra GLU immunoreactive positive cells induced by rotenone. 4. Nicotine antagonizes the decrease of expression of rat midbrain substantia nigra GABA immunoreactive positive cells induced by rotenone.Rotenone treated rats in 2 weeks, 4 weeks, 5 weeks, the expression of rat midbrain substantia nigra GABA immunoreactive positive cells were less than the control group(P < 0.05), however, the expression of GABA in rats that pretreated with different doses of nicotine(0.5, 1.0 mg/kg) were increased contrast to the rotenone group(P < 0.05), but there were no differences in two different concentrations of nicotine treatment(P > 0.05). This suggests that nicotine can antagonize the decrease of expression of rat midbrain substantia nigra GABA immunoreactive positive cells induced by rotenone. Conclusion:Nicotine can antagonize the change that the GLUergic neurons increased and GABAergic neurons decreased in the midbrain substantia nigra of the development process of Parkinson's disease rats induced by rotenone.