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[Relationship between P-type Na+ -K+ -Atpase and migraine: an experimental study with rats]
Yi-min Hu1, Xiao-su Yang, Chang-ying Zhang
1Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China.
Objective:
To investigate the role of P-type Na+ -K+ -ATPase in the mechanism of migraine.
Methods:
nitroglycerin induced migraine Twenty Sprague-Dawley rats, 10 male and 10 female, were randomly divided into 2 groups: model group, undergoing subcutaneous injection of nitroglycerin 10 mg/kg once a week for 4 weeks so as to establish migraine model, and control group, undergoing subcutaneous injection of normal saline. Then the rats were killed with their trigeminal ganglia, trigeminocervical complex, and cortex of frontal lobe taken out. RT-PCR and Western-blotting were used to detect the mRNA and protein expression of P-type Na+ -K+ -ATPase. Immuno-precipitation assay was conducted to observe the Na+ -K+ -ATPase activity. The concentration of intracellular Ca2+ was investigated by Fluo-3/AM fluorometric method.
Results:
The mRNA and protein expression levels and activity of P-type Na+ -K+ -ATPase in the trigeminal ganglion and trigeminocervical complex of the model group were 0.72 +/- 0.05, 0.59 +/- 0.05, and 5.21 +/- 0.51 respectively, and the mRNA and protein expression levels and activity of P-type Na+ -K+ -ATPase in the cortex of frontal lobe of the model group were 0.70 +/- 0.05, 0.60 +/- 0.05, and 3.61 +/- 0.49 respectively, all significantly lower than those of the control group (0.83 +/- 0.10, 0.67 +/- 0.06, 6.53 +/- 0.73, 0.81 +/- 0.08, 0.71 +/- 0.09, and 6.61 +/- 0.73 respectively, all P < 0.05). The concentration of intracellular Ca2 in trigeminal ganglion and trigeminocervical complex and the concentration of Ca2+ in the cortex of frontal lobe of the model group were 211,182 +/- 12,973 and 186,511 +/- 18,297 respectively, both significantly higher than those of the control group (135,243 +/- 18,105 and 143,289 25,175 respectively, both P < 0.01).
Conclusion:
P-type Na+ -K+ -ATPase may infect the pathogenesis of migraine by its expression and activity.

