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Objective To explore the effects of flunarizine hydrochloride on plasma calcitonin gene-related pep-tide and substance P levels after CSD in a rat migraine model of cortical spreading depression (CSD). Methods Thirty adult rats were randomly and evenly divided into three groups:control Group, CSD group and flunarizine group. The CSD waves were evoked by application of potassium chloride on brain surface with filter paper. Funarizine hydrochloride was intravenously administered to rats five minutes prior to application of potassium chloride. The plasma levels of CGRP and SP were measured by using radioimmunity assay. Statistical analyses were performed using two-sample t test and analy-sis of variance. Results CSD waves were absent in control group whereas CSD waves were induced in CSD and flunari-zine groups. The latency of the first CSD wave was longer in flunarizine group (167.90 ± 25.18 s) than in CSD group (130.90 ± 13.30 s) (P<0.01). The number of CSD waves was smaller in flunarizine group (4.50 ± 1.84) than in CSD group (8.50 ± 2.07) (P<0.01). The amplitude of CSD waves was lower in flunarizine group (11.40 ± 4.12 mv) than in CSD group (24.40±3.57 mv) (P<0.01). The levels of CGRP and SP in both CSD group (CGRP, 32.95±11.61 pg/mL;SP, 27.80±7.51 pg/mL) and flunarizine group (CGRP, 25.13 ± 5.67 pg/mL; SP, 19.45 ± 6.10 pg/mL) were higher than in control group (CGRP, 14.44 ± 6.39 pg/mL; SP, 12.36 ± 4.22 pg/mL) (P<0.01). The levels of CGRP and SP in flunarizine group (CGRP, 25.13±5.67 pg/mL;SP, 19.45±6.10 pg/mL) were lower than those in CSD group (CGRP, 32.95±11.61 pg/mL;SP, 27.80± 7.51 pg/mL) (P<0.05). Conclusions Flunarizine hydrochloride can inhibit CSD and reduce the plama levels of CGRP and SP in the rat model of CSD.
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<p><b>BACKGROUND</b>The molecular and cellular origins of migraine headache are among the most complex problems in contemporary neurology. Up to now the pathogenesis of migraine still remains unclearly defined. The objective of this study was to explore new factors that may be related to the mechanism of migraine.</p><p><b>METHODS</b>The present study performed a comprehensive analysis of gene expression in the trigeminal nucleus caudalis induced by electrical stimulation of dura mater surrounding the superior sagittal sinus in conscious rats using microarray analysis followed by quantitative real-time reverse-transcribed polymerase chain reaction (qRT-PCR) verification. Student's two sample t-test was employed when two groups were compared. A P value <0.05 was considered to be statistically significant.</p><p><b>RESULTS</b>Comparing the placebo and the electrical stimulation groups, 40 genes were determined to be significantly differentially expressed. These significantly differentially expressed genes were involved in many pathways, including transporter activity, tryptophan metabolism, G protein signaling, kinase activity, actin binding, signal transducer activity, anion transport, protein folding, enzyme inhibitor activity, coenzyme metabolism, binding, ion transport, cell adhesion, metal ion transport, oxidoreductase activity, mitochondrion function, and others. Most of the genes were involved in more than 2 pathways. Of particular interest is the up-regulation of Phactr3 and Akap5 and the down-regulation of Kdr.</p><p><b>CONCLUSION</b>These findings may provide important clues for a better understanding of the molecular mechanism of migraine.</p>
Assuntos
Animais , Masculino , Ratos , Dura-Máter , Fisiologia , Estimulação Elétrica , Expressão Gênica , Fisiologia , Análise em Microsséries , Transtornos de Enxaqueca , Genética , Ratos Sprague-Dawley , Reação em Cadeia da Polimerase em Tempo Real , Seio Sagital Superior , FisiologiaRESUMO
Objective To determine whether rizatriptan has an effect on cortical spreading depression (CSD) and c-Fos expression within periaqueductal grey (PAG) induced by CSD in rats. Methods The experimental SD rats were randomly divided into group A injected with KCl, group B KCl plus rizatriptan and group C NaCL The number and amplitude of CSD were recorded after KCl or NaCl injection. C-Fos positive neurons of different layer were identified by the immunohistochemical technique 2 hours after the first injection of KCl or NaCl. Results There was no CSD in group C. The number of CSD in group A ( 10.70±3.23 ) was significantly more than that in group B (6.10±2.56, t = - 3.528, P < 0.01 ). The amplitude of CSD in group A ( 17.33 (95% CI 11.45--23.11 ) mV) was significantly greater than that in group B (11.82 (95%CI 9.24--14.70) mV, Z= -4.360, P< 0.01). There were more cFos-like immnoreactive neurons in every layer in group A than in group C (P < 0.01 ) and in group B (P < 0.05 ). Conclusion Rizatriptan has an inhibitory effect on CSD, which might induce the headache through exciting the neurons in PAG.
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Objective To observe the clinical features of migraine based on out-patient clinic data and provide help for the diagnosis and treatment of migraine. Methods In a retrospective study of 309 patients with migraine, we investigated the clinical characteristics of migraine of both genders and different types, and the risk factors for MOH transformed from migraine. Results The female to male ratio was about 3:1,76.1% of the patients had triggering factors. The most common characteristics of headache were moderate to severe intensity of the pain (97.7%), aggravation by routine physical activity (75.1%), and association with nausea (90.9%) and/or vomiting (70.6%). There were significant differences in some clinical characteristics of migraine in females as compared with these in males and in patients with migraine without aura (MWOA) as compared with those with aura (MWA). The risk factors for MOH transformed from migraine were elder age of onset, high attack frequency and the analgesics frequently used (P < 0.05).Conclusion It is suggested that carefully collecting the characteristics of headache, triggering factors and therapeutic history is the foundation of correct diagnosis and effective treatment for migraine.
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@#In recent years,many investigations manifested that cortical spreading depression was probably the physiologic foundation of migraine aura.The authors reviewd the relationship between migraine aura and cortical spreading depression.