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机构地区:[1]皖南医学院细胞电生理研究室,安徽芜湖241002
出 处:《皖南医学院学报》2007年第4期241-244,共4页Journal of Wannan Medical College
基 金:国家自然科学基金项目(30270366);安徽省自然科学基金项目(050430401)
摘 要:目的:探讨代谢型谷氨酸受体(mGluRs)对离体脊髓背根向运动神经元(MN)传人的调制作用。方法:应用新生大鼠(8~14d)脊髓切片MN细胞内记录技术,观察mGluRs广谱激动剂反式-1-氨基-1,3-环戊烷二羧酸(ACPD)对背根(DR)电刺激诱发兴奋性突触后电位(EPSP)的影响。结果:对离体脊髓切片灌流ACPD(5~25μmol/L)15~20min,在11个测试的MN,能可逆性抑制DR刺激诱发的EPSP(即DR—EPSP)的幅度(P〈0.01)和曲线下面积(P〈0.05)。在用抑制性氨基酸受体拮抗剂印防己毒素和士的宁预处理后,DR—EPSP仍能被10μmol/LACPD显著性抑制(P〈0.05,n=3)。结论:ACPD可激活mGluRs而抑制脊髓DR向MN的兴奋性突触传递,其机制可能不涉及增强弘氨基丁酸A受体或甘氨酸受体的作用机制。Objective : To evaluate the modulatory process of metabotropic glutamate receptors (mGluRs) on excitatory postsynaptic potential (EPSP) evoked by dorsal root (DR) stimulation in neonatal rat spinal cord slices. Methods: The intracellular recordings were made in motoneurons (MNs) of spinal cord slices isolated from neonatal rats (8- 14 days old). Results: The DR-EPSPs in 11 tested MNs were reversibly suppressed in amplitude ( P 〈 0.01 ) and area under curve ( P 〈 0.05 ) by superfusion of mGluRs agonist trans-( 1S, 3R)-1-amino-1,3-cyclopentanedicarboxylic acid (ACPD,5-25 μmol/L) in a duration of 15 min. DR-EPSPs in 3 MNs were significantly inhibited by ACPD at 10 μmol/L (P〈 0.05) in the presence of picrotoxin (30 μmol/L) and strychnine( 1.0 μmol/L), antagonist of γ-aminobutyric acid A (GABAA) receptor and glyeine receptor, respectively. Conclusion: ACPD could modulate the excitatory postsynaptic potential in the pathways of DR to MNs by activation of mGluRs, and its action may not involve the potenti- ation mechanism of GABAA or glycine receptors.
关 键 词:运动神经元 代谢型谷氨酸受体 背根 突触传递 印防己毒素 士的宁 反式-1-氨基-1 3-环戊烷二羧酸
分 类 号:R338.1[医药卫生—人体生理学]
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