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牛磺酸对三叉神经尾侧亚核胶状质神经元甘氨酸和突触外GABA(A)受体的激活作用。

Activation of glycine and extrasynaptic GABA(A) receptors by taurine on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis.

作者信息

Nguyen Thi Thanh Hoang, Bhattarai Janardhan Prasad, Park Soo Joung, Han Seong Kyu

机构信息

Department of Oral Physiology & Institute of Oral Bioscience, School of Dentistry, Chonbuk National University, Jeonju 561-756, Republic of Korea.

出版信息

Neural Plast. 2013;2013:740581. doi: 10.1155/2013/740581. Epub 2013 Nov 28.

Abstract

The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) has been known for the processing and transmission of orofacial nociceptive information. Taurine, one of the most plentiful free amino-acids in humans, has proved to be involved in pain modulation. In this study, using whole-cell patch clamp technique, we investigated the direct membrane effects of taurine and the action mechanism behind taurine-mediated responses on the SG neurons of the Vc. Taurine showed non-desensitizing and repeatable membrane depolarizations and inward currents which remained in the presence of amino-acid receptors blocking cocktail (AARBC) with tetrodotoxin, indicating that taurine acts directly on the postsynaptic SG neurons. Further, application of taurine at different doses (10  μM to 3 mM) showed a concentration dependent depolarizations and inward currents with the EC50 of 84.3  μM and 723  μM, respectively. Taurine-mediated responses were partially blocked by picrotoxin (50  μM) and almost completely blocked by strychnine (2  μM), suggesting that taurine-mediated responses are via glycine receptor (GlyR) activation. In addition, taurine (1 mM) activated extrasynaptic GABA(A) receptor (GABA(A)R)-mediated currents. Taken together, our results indicate that taurine can be a target molecule for orofacial pain modulation through the activation of GlyRs and/or extrasynaptic GABA(A)Rs on the SG neurons.

摘要

三叉神经尾侧亚核(Vc)的胶状质(SG)在口腔面部伤害性信息的处理和传递方面已为人所知。牛磺酸是人体内含量最丰富的游离氨基酸之一,已被证明参与疼痛调节。在本研究中,我们使用全细胞膜片钳技术,研究了牛磺酸对Vc的SG神经元的直接膜效应以及牛磺酸介导反应背后的作用机制。牛磺酸表现出不脱敏且可重复的膜去极化和内向电流,在存在用河豚毒素的氨基酸受体阻断混合物(AARBC)的情况下这些仍存在,表明牛磺酸直接作用于突触后SG神经元。此外,应用不同剂量(10 μM至3 mM)的牛磺酸显示出浓度依赖性的去极化和内向电流,其EC50分别为84.3 μM和723 μM。牛磺酸介导的反应被印防己毒素(50 μM)部分阻断,几乎被士的宁(2 μM)完全阻断,这表明牛磺酸介导的反应是通过甘氨酸受体(GlyR)激活。此外,牛磺酸(1 mM)激活了突触外γ-氨基丁酸A受体(GABA(A)R)介导的电流。综上所述,我们的结果表明,牛磺酸可通过激活SG神经元上的GlyRs和/或突触外GABA(A)Rs成为口腔面部疼痛调节的靶分子。

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