褪黑素对戊四氮致癫痫大鼠海马谷氨酸受体和γ-氨基丁酸受体的影响  

AInfluence of melatonin on N-methyl-D-aspartate receptorζ1 and γ-aminobu tyric acid-A receptor α1 in hippocampus of pentylenetetrazole-induced epileptic rats

作　　者：孙秋云[1] 张哓琴 

机构地区：[1]武汉大学中南医院神经科,湖北省武汉市430071

出　　处：《中国临床康复》2004年第13期2464-2465,共2页Chinese Journal of Clinical Rehabilitation

摘　　要：目的:探讨褪黑素抗癫痫的机制。方法:应用SP法研究戊四氮致癫痫大鼠和褪黑素抗癫痫大鼠海马谷氨酸受体ζ1(N-methyl-D-aspartaterecepterζ1,NMDAζ1)和γ-氨基丁酸受体Aα1(r-aminobutyricacid-Arecepterα1,GABAARα1)的变化。结果:海马NMDAζ1表达在戊四氮致癫痫组明显高于正常对照组(q吸光度=6.34,P<0.01;q阳性率=9.394,P<0.01),褪黑素抗癫痫组明显低于戊四氮致癫痫组(q吸光度=6.01,P<0.01;q阳性率=9.000,P<0.01),褪黑素抗癫痫组与正常对照组之间差异无显著性意义(q吸光度=0.032,P>0.05;q阳性率=0.4015,P>0.05);海马GABAARα1表达在戊四氮致癫痫组明显低于正常对照组(q吸光度=4.65,P<0.01;q阳性率=5.3,P<0.01),褪黑素抗癫痫组明显高于戊四氮致癫痫组(q吸光度=4.58,P<0.01;q吸光度=5.21,P<0.01),褪黑素抗癫痫组与正常对照组之间差异无显著性意义(q吸光度=0.07,P>0.05;q吸光度=0.097,P>0.05)。结论:褪黑素可能通过抑制海马兴奋性神经递质受体NMDAζ1和激活海马抑制性神经递质受体GABAARα1的活性与表达,降低大脑皮质的兴奋性,抑制癫痫的形成及发展来发挥抗癫痫作用。AIM:To explore the possible antiepileptic mechanism of melatonin. METHODS:The expressions of N-methyl-D-aspartate receptorζ1 (NMDAζ1) and γ-aminobutyric acid-A receptor α1(GABAARα1) in the hippocampus of pentylene tetrazole(PTZ)-induced epileptic rats and epileptic rats treated with melatonin were determined by SP method. RESULTS:The expression of NMDAζ1 in the hippocampus of PTZ group rats was hig her than that of control group rats(absorbance: q=6.34,P< 0.01;positive rate:q=9 .394,P< 0.01).After treatment with melatonin,the NMDAζ1 expression was decreas ed significantly(absorbance:q=6.01,P< 0.01;positive rate:q=9.000,P< 0.01).The re was no significant difference in the expression of NMDAζ1 between the rats o f melatonin group and normal control group(absorbance:q=0.032,P >0.05;positive rate:q=0.401 5,P >0.05).The expression of GABAARα1 in the hippocampus of PTZ group rats was lower than that of control group rats(absorbance:q=4.65,P< 0.01 ;positive rate:q=5.3,P< 0.01).After treatment with melatonin, the expression o f GABAARα1 was increased significantly(absorbance:q=4.58,P< 0.01;positive rate :q=5.21,P< 0.01). There was also no significant difference between the rats of melatonin group and normal control group(absorbance:q=0.07,P >0.05;positive r ate: q=0.097,P >0.05). CONCLUSION:Melatonin may reduce the excitability of cerebral cortices by inhib iting the activities of NMDAζ1 and by promoting the activities of GABAARα1 in the hippocampus,so the development and formation f epilepsy are inhibited.

关 键 词：褪黑素 戊四氮 癫痫 大鼠 海马 谷氨酸受体 Γ-氨基丁酸受体 

分 类 号：R742.1[医药卫生—神经病学与精神病学]