Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)
Prostaglandin E2 (PGE2) inhibits glutamatergic synaptic transmission in dorsolateral periaqueductal gray (dl-PAG)
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DOI：
10.1016/j.brainres.2007.06.004
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发表时间：
2007-08-08
期刊：
影响因子：
2.9
通讯作者：
Li, Jianhua
中科院分区：
文献类型：
--
作者：
Lu, Jian;Xing, Jihong;Li, Jianhua
本研究的目的是确定前列腺素 E-2 (PGE(2)) 通过兴奋性和抑制性突触输入调节背外侧导水管周围灰质 (dl-PAG) 神经元活动的作用。首先，进行全细胞电压钳记录以获得 dl-PAG 神经元的兴奋性和抑制性突触后电流（EPSC 和 IPSC）。我们的结果表明，PGE(2) 显着降低了微型 EPSC 的频率和诱发 EPSC 的幅度。磺前列酮（Sulprostone）是一种 PGE(2) EP3 受体激动剂，可以模拟这种作用。相比之下，PGE(2)对IPSCs没有明显影响。此外，使用全细胞电流钳方法记录了 dl-PAG 神经元的自发动作电位。 PGE(2)显着减弱了dl-PAG神经元的放电率。在谷氨酸 NMDA 和非 NMDA 受体拮抗剂存在下，放电活性的降低被消除。目前的研究结果提供了第一个证据，表明 PGE(2) 通过选择性减弱谷氨酸突触输入来抑制 dl-PAG 的神经元活动，这可能是由于突触前 EP3 受体的激活。 (c) 2007 Elsevier B.V. 保留所有权利。
The purpose of this study was to determine the role of prostaglandin E-2 (PGE(2)) in modulating neuronal activity of the dorsolateral periaqueductal gray (dl-PAG) through excitatory and inhibitory synaptic inputs. First, whole cell voltage-clamp recording was performed to obtain excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) of the dl-PAG neurons. Our results show that PGE(2) significantly decreased the frequency of miniature EPSCs and amplitude of evoked EPSCs. The effects were mimicked by sulprostone, an agonist to PGE(2) EP3 receptors. In contrast, PGE(2) had no distinct effect on IPSCs. In addition, spontaneous action potential of the dl-PAG neurons was recorded using whole cell current-clamp methods. PGE(2) significantly attenuated the discharge rate of the dl-PAG neurons. The decreased firing activity was abolished in the presence of glutamate NMDA and non-NMDA receptor antagonists. The results from the current study provide the first evidence indicating that PGE(2) inhibits the neuronal activity of the dl-PAG via selective attenuation of glutamatergic synaptic inputs, likely due to the activation of presynaptic EP3 receptors. (c) 2007 Elsevier B.V. All rights reserved.