| Objective:1, To authenticate the feasibility of the migraine animal model simulating the migraine attacks by using chemical stimulation on the superior sagittal sinus.2, To study the role of NF-κB protein on the nociceptive transmission of migraine attacks.Methods:1 , Forty male Sprague-Dawley rats, weighing 220~ 250g, were randomly divided into four groups: the blank(n=10), control(n=10) ,capsaicin 1μM (n=10)and capsaicin 10μM group(n=10). The rats of blank group were killed after anesthetized excessively. The rats remained were drilled on their cranium by platform bur to expose the superior sagittal sinus (SSS),and dropped distilled water(75% alcohol in it,the percent is 6%), capsaicin 1μM and capsaicin 10μM about 0.1ml seperately。 One hour later, the rats were paralyzed and perfused to fix, which the brainstem were removed and post-fixed. Coronal sections through the midbrain PAG were cut and the expression of c-fos immuno-reactivity was detected with standard avidin-biotin peroxidase immunohistochemical techniques.2, Seventy male Sprague-Dawley rats, weighing 220~ 250g, were randomly divided into seven groups: the blank(n= 10) , sham-operated(n=10) , stimulated(n=10), sumatriptan(n=10), normal sodium A(n=10), flunarizine (n=10), normal sodium B group(n=10). Ten days before we gave flunarizine (1 mg/mL, 1 mg/Kg ) and normal sodium (1 ml/Kg ) separately to the rats of flunarizine and normal sodium B groups by intraperitoneal injection. The rats of blank group were killed after anesthetized excessively. The rats remained were drilled on their cranium by platform bur to expose the superior sagittal sinus (SSS), and a pair of electrodes were placed on the SSS gently. The dura mater near the SSS of rats in the stimulated group was stimulated with square wave current (250us, 1.5mA, 3 HZ) for 2 hours after the operation. sumatriptanand normal sodium A group were separately given the 5-HTjd receptor agonist-sumatriptan (lmg/mL,lmg/Kg) and normal sodium (1 ml/Kg) by intraperitoneal injection after stimulating 30 minutes. No rat was stimulated in the sham-operated group. One hour later, the rats were paralyzed and perfused to fix, which the brainstem were removed and post-fixed. Coronal sections through the midbrain PAG were cut and the expression of NF-kB irnrnuno-reactivity was detected with standard avidin-biotin peroxidase immunohistochemical techniques.Results:1 ^ The number of Fos positive neurons in capsaicin lOuM and luM group were increased markedly compared with that in blank group and control group respectively;capsaicin lOuM group was also increased markedly compared with capsaicin luM group;and there was no significant difference between blank group and control group.2^ The number of NF-kB positive neurons in stimulated group was increased markedly compared with that in blank,sham-operated,sumatriptan and flunarizine group respectively. The number of NF-kB positive neurons in sumatriptan group was decreased markedly compared with that in normal sodium A group. The number of NF-kB positive neurons in flunarizine group was decreased markedly compared with that in normal sodium B group,and there was no significant difference between blank and sham-operated groups. The number of NF-kB positive neurons was also no significant difference between stimulated group and both normal sodium groups.Conclusion:1 -. The PAG could be activated by the capsaicin chemical stimulation of the dura mater near the SSS. The migraine animal model by using chemical stimulation of capsaicin simulated the general process of migrain attacks. This migraine animal model is feasibile.2> The NF-kB positive neuros were activated in the PAG by electric stimulation of the dura mater near the SSS . NF-kB protein could be involved in the processing of nociceptive signals on migraine attacks.The expression of NF-kB protein could be accommodated by the 5-HTid receptor agonist andchannel blocker of the calcium . |