中华神经科杂志
中華神經科雜誌
중화신경과잡지
Chinese Journal of Neurology
2013年
7期
479-482
,共4页
范袆%杨晓苏%郭一航%周经纬
範袆%楊曉囌%郭一航%週經緯
범위%양효소%곽일항%주경위
偏头痛%受体,GABA-A%RNA,信使%脑干%三叉神经%丙戊酸
偏頭痛%受體,GABA-A%RNA,信使%腦榦%三扠神經%丙戊痠
편두통%수체,GABA-A%RNA,신사%뇌간%삼차신경%병무산
Migraine disorders%Receptor,GABA-A%RNA,messenger%Brain stem%Trigeminal nerve%Valproic acid
目的 利用硝酸甘油所致偏头痛大鼠模型探讨γ-氨基丁酸A(GABAA)受体α1亚基mRNA在偏头痛大鼠脑干及三叉神经组织中的表达变化.方法 30只成年雌性SD大鼠按完全随机分组方法分为对照组、模型组和丙戊酸钠干预组,后两组又随机分发作期和间歇期两个亚组(每组各6只).模型组及丙戊酸钠干预组按Cristina法复制偏头痛大鼠模型(每周1次,连续5周),干预组于第2次造模后每天灌服0.5 g/L的丙戊酸钠2次,共10 mL/kg；对照组和模型组于第2次造模后每天灌服生理盐水2次,共10 ml/kg.第5次造模后用逆转录-聚合酶链反应法测定大鼠脑干及三叉神经组织中GABAA受体α1亚基mRNA的表达.结果 模型组发作期的GABAA受体α1亚基mRNA的表达(1.50±0.13)均高于其他各组(对照组1.01±0.24,模型组间歇期1.04±0.10,干预组发作期0.99±0.22,干预组间歇期0.72±0.03),但仅与模型组间歇期相比差异有统计学意义(x2=9.490,P =0.009)；模型组与对照组、干预组的发作期及间歇期相比差异无统计学意义,干预组的发作期及间歇期与对照组相比差异无统计学意义.结论 偏头痛的发生可能与GABAA受体α1亚基在mRNA水平的表达上调有关.
目的 利用硝痠甘油所緻偏頭痛大鼠模型探討γ-氨基丁痠A(GABAA)受體α1亞基mRNA在偏頭痛大鼠腦榦及三扠神經組織中的錶達變化.方法 30隻成年雌性SD大鼠按完全隨機分組方法分為對照組、模型組和丙戊痠鈉榦預組,後兩組又隨機分髮作期和間歇期兩箇亞組(每組各6隻).模型組及丙戊痠鈉榦預組按Cristina法複製偏頭痛大鼠模型(每週1次,連續5週),榦預組于第2次造模後每天灌服0.5 g/L的丙戊痠鈉2次,共10 mL/kg；對照組和模型組于第2次造模後每天灌服生理鹽水2次,共10 ml/kg.第5次造模後用逆轉錄-聚閤酶鏈反應法測定大鼠腦榦及三扠神經組織中GABAA受體α1亞基mRNA的錶達.結果 模型組髮作期的GABAA受體α1亞基mRNA的錶達(1.50±0.13)均高于其他各組(對照組1.01±0.24,模型組間歇期1.04±0.10,榦預組髮作期0.99±0.22,榦預組間歇期0.72±0.03),但僅與模型組間歇期相比差異有統計學意義(x2=9.490,P =0.009)；模型組與對照組、榦預組的髮作期及間歇期相比差異無統計學意義,榦預組的髮作期及間歇期與對照組相比差異無統計學意義.結論 偏頭痛的髮生可能與GABAA受體α1亞基在mRNA水平的錶達上調有關.
목적 이용초산감유소치편두통대서모형탐토γ-안기정산A(GABAA)수체α1아기mRNA재편두통대서뇌간급삼차신경조직중적표체변화.방법 30지성년자성SD대서안완전수궤분조방법분위대조조、모형조화병무산납간예조,후량조우수궤분발작기화간헐기량개아조(매조각6지).모형조급병무산납간예조안Cristina법복제편두통대서모형(매주1차,련속5주),간예조우제2차조모후매천관복0.5 g/L적병무산납2차,공10 mL/kg；대조조화모형조우제2차조모후매천관복생리염수2차,공10 ml/kg.제5차조모후용역전록-취합매련반응법측정대서뇌간급삼차신경조직중GABAA수체α1아기mRNA적표체.결과 모형조발작기적GABAA수체α1아기mRNA적표체(1.50±0.13)균고우기타각조(대조조1.01±0.24,모형조간헐기1.04±0.10,간예조발작기0.99±0.22,간예조간헐기0.72±0.03),단부여모형조간헐기상비차이유통계학의의(x2=9.490,P =0.009)；모형조여대조조、간예조적발작기급간헐기상비차이무통계학의의,간예조적발작기급간헐기여대조조상비차이무통계학의의.결론 편두통적발생가능여GABAA수체α1아기재mRNA수평적표체상조유관.
Objective To investigate the change of gamma-aminobutyric acid A (GABAA) receptor α1 subunit mRNA expression in nitroglycerin induced migraine rat model,thus suggesting the relationship between GABAA receptor and migraine.Methods Thirty adult female Sprague-Dawley (SD) rats were randomly divided into control group,migraine model group,sodium valproate-treated group,each of the last 2 groups was divided into the attacking group and intermission group.The model of migraine was established using Cristina method,once a week for 5 weeks.After the second injection,rats in sodium valproate-treated group were given sodium valproate(0.5 g/L,10 ml/kg) everyday,and those in control group and model group were given normal saline solution(10 ml/kg).After the fifth injection,at the second hour(attacking groups) or the fourth day(intermission groups and control group),reverse transcription-polymerase chain reaction was used to detect the expression level of GABAA receptor α1 mRNA in brainstem and trigeminal ganglion.Results The expression level of GABAA receptor α1 mRNA in modeling attacking group(1.50 ±0.13) was higher than any other group(control group:1.01 ±0.24,modeling intermission group:1.04 ±0.10,sodium valproate-treated attacking group:0.99 ± 0.22,sodium valproate-treated intermission group:0.72 ± 0.03),and it was significantly higher than modeling intermission group(x2 =9.490,P =0.009).There was no statistical difference between modeling group and any other group,and compared with control group,there was no statistical difference in sodium valproate-treated attacking group or intermission group.Conclusion The pathogenesis of migraine may be related to the expression level of GABAA receptor α1 mRNA.
