Department of Physiology and Neurobiology, Xinxiang Medical University, Xinxiang, Henan Province, People's Republic of China.
Neurol Sci. 2014 Apr;35(4):551-7. doi: 10.1007/s10072-013-1543-1. Epub 2013 Sep 22.
This study aimed to establish a model of synaptic plasticity by the activation of metabotropic glutamate receptor (mGluR) I in rat medial septal diagonal band (MSDB). Electrophysiological experiment was performed to record the theta frequency oscillation activities in rat MSDB slices. The data were recorded and analyzed with Spike 2 (CED, Cambridge, UK). Application of aminocyclopentane-1, 3-dicarboxylic acid (ACPD) to MSDB slices produced theta frequency oscillations (4-12 Hz) which persisted for hours after ACPD washout, suggesting the existence of a form of synaptic plasticity in long-term oscillations (LTOs). Addition of NMDA receptor antagonist AP5 (50 μM) caused no significant change in area power. In contrast, AMPA/Kainate receptor antagonist NBQX administration partially reduced the area power. Infusion of ZD7288, a hyperpolarization-activated channel (Ih) inhibitor, caused additional reduction to control level. Comparable effects were also observed with administration of DHPG (3, 5-dihydroxyphenylglycine) which also elicited LTOs. mGluR I activation induced theta oscillation and this activity maintained hours after drug washout. Both AMPA and hyperpolarization-activated channel make an essential contribution to LTO. Our study herein established a model of synaptic plasticity.
本研究旨在通过激活大鼠中隔斜角带(MSDB)中的代谢型谷氨酸受体(mGluR)I 来建立突触可塑性模型。电生理实验用于记录大鼠 MSDB 切片中的θ频率振荡活动。Spike 2(CED,英国剑桥)用于记录和分析数据。ACPD 应用于 MSDB 切片会产生θ频率振荡(4-12 Hz),在 ACPD 冲洗后持续数小时,表明存在长期振荡(LTO)形式的突触可塑性。NMDA 受体拮抗剂 AP5(50 μM)的添加对面积功率没有显著影响。相比之下,AMPA/KA 受体拮抗剂 NBQX 的给药部分减少了面积功率。超极化激活通道(Ih)抑制剂 ZD7288 的输注导致对照水平的进一步降低。给予 3,5-二羟基苯甘氨酸(DHPG)也会引起类似的效果,DHPG 也会引发 LTO。mGluR I 的激活诱导θ振荡,这种活动在药物冲洗后持续数小时。AMPA 和超极化激活通道都对 LTO 做出了重要贡献。我们的研究在此建立了一个突触可塑性模型。