Xing Jihong, Lu Jian, Li Jianhua
The First Clinical Hospital, Jilin University Norman Bethune College of Medicine, Changchun, Jilin 130021, People's Republic of China.
Neurosci Lett. 2009 May 8;455(1):8-13. doi: 10.1016/j.neulet.2009.03.063. Epub 2009 Mar 24.
The purpose of this study was to determine the role of angiotensin II (Ang II) in modulating inhibitory and excitatory synaptic inputs to the dorsolateral periaqueductal gray (dl-PAG). The whole cell voltage-clamp recording was performed to examine inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs) of the dl-PAG neurons. Ang II, at the concentration of 2microM, decreased the frequency of miniature IPSCs from 0.83+/-0.02 to 0.45+/-0.03Hz (P<0.05) in 10 tested neurons. This did not significantly affect the amplitude and decay time constant. The effect of Ang II on miniature IPSCs was blocked by the prior application of Ang II AT1 receptor antagonist losartan, but not by AT2 receptor antagonist PD123319. Additionally, Ang II decreased the amplitude of evoked IPSCs from 148+/-15 to 89+/-7pA (P<0.05), and increased the paired-pulse ratio from 96+/-5% to 125+/-7% (P<0.05) in eight tested neurons. In contrast, Ang II had no distinct effects on the EPSCs. Our data suggest that Ang II inhibits GABAergic synaptic inputs to the dl-PAG through activation of presynaptic AT1 receptors.
本研究的目的是确定血管紧张素II（Ang II）在调节背外侧导水管周围灰质（dl-PAG）的抑制性和兴奋性突触输入中的作用。采用全细胞电压钳记录技术检测dl-PAG神经元的抑制性和兴奋性突触后电流（IPSCs和EPSCs）。在10个受试神经元中，2μM浓度的Ang II使微小IPSCs的频率从0.83±0.02Hz降至0.45±0.03Hz（P<0.05）。这对幅度和衰减时间常数没有显著影响。Ang II对微小IPSCs的作用可被预先应用的Ang II AT1受体拮抗剂氯沙坦阻断，但不能被AT2受体拮抗剂PD123319阻断。此外，在8个受试神经元中，Ang II使诱发IPSCs的幅度从148±15pA降至89±7pA（P<0.05），并使配对脉冲比率从96±5%增加到125±7%（P<0.05）。相反，Ang II对EPSCs没有明显影响。我们的数据表明，Ang II通过激活突触前AT1受体抑制dl-PAG的GABA能突触输入。
