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胃饥饿素对大鼠海马细胞电压依赖性钾电流的抑制作用未受影响。

NO involvement in the inhibition of ghrelin on voltage-dependent potassium currents in rat hippocampal cells.

作者信息

Lu Yong, Dang Shaokang, Wang Xu, Zhang Junli, Zhang Lin, Su Qian, Zhang Huiping, Lin Tianwei, Zhang Xiaoxiao, Zhang Yurong, Sun Hongli, Zhu Zhongliang, Li Hui

机构信息

Department of Neonatology, the First Affiliated Hospital of Xi'an Jiaotong University, Shanxi 710061, China; Center Laboratory, Heze Medical College, Shandong 274000, China.

Department of Neonatology, the First Affiliated Hospital of Xi'an Jiaotong University, Shanxi 710061, China.

出版信息

Brain Res. 2018 Jan 1;1678:40-46. doi: 10.1016/j.brainres.2017.09.031. Epub 2017 Oct 4.

Abstract

Ghrelin is a peptide hormone that plays an important role in promoting appetite, regulating distribution and rate of use of energy, cognition, and mood disorders, but the relevant neural mechanisms of these function are still not clear. In this study, we examined the effect of ghrelin on voltage-dependent potassium (K) currents in hippocampal cells of 1-3 days SD rats by whole-cell patch-clamp technique, and discussed whether NO was involved in this process. The results showed that ghrelin significantly inhibited the voltage-dependent K currents in hippocampal cells, and the inhibitory effect was more significant when l-arginine was co-administered. In contrast, N-nitro- l-arginine methyl ester increased the ghrelin inhibited K currents and attenuated the inhibitory effect of ghrelin. While d-arginine (D-AA) showed no significant impact on the ghrelin-induced decrease in K current. These results show that ghrelin may play a physiological role by inhibiting hippocampal voltage dependent K currents, and the NO pathway may be involved in this process.

摘要

胃饥饿素是一种肽类激素,在促进食欲、调节能量分布和利用速率、认知及情绪障碍方面发挥重要作用,但其这些功能相关的神经机制仍不清楚。在本研究中,我们采用全细胞膜片钳技术检测了胃饥饿素对1至3日龄SD大鼠海马细胞中电压依赖性钾(K)电流的影响,并探讨了一氧化氮(NO)是否参与此过程。结果显示,胃饥饿素显著抑制海马细胞中的电压依赖性K电流,当共同给予L-精氨酸时,抑制作用更显著。相反,N-硝基-L-精氨酸甲酯增加了胃饥饿素抑制的K电流,并减弱了胃饥饿素的抑制作用。而D-精氨酸(D-AA)对胃饥饿素诱导的K电流降低无显著影响。这些结果表明,胃饥饿素可能通过抑制海马电压依赖性K电流发挥生理作用,且NO途径可能参与此过程。

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