Wagner Lysann, Warwick Rebekah A, Pannicke Thomas, Reichenbach Andreas, Grosche Antje, Hanani Menachem
Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig, Jahnallee 59, 04109 Leipzig, Germany.
Laboratory of Experimental Surgery, Hadassah Hebrew University Medical Center, Mount Scopus, Jerusalem 91240, Israel.
Neurosci Lett. 2014 Aug 22;578:143-7. doi: 10.1016/j.neulet.2014.06.047. Epub 2014 Jun 30.
It has been proposed that glutamate serves as a mediator between neurons and satellite glial cells (SGCs) in sensory ganglia and that SGCs release glutamate. Using a novel method, we studied glutamate release from SGCs from murine trigeminal ganglia. Sensory neurons with adhering SGCs were enzymatically isolated from wild type and transgenic mice in which vesicular exocytosis was suppressed in glial cells. Extracellular glutamate was detected by microfluorimetry. After loading the cells with a photolabile Ca(2+) chelator, the intracellular Ca(2+) concentration was raised in SGCs by a UV pulse, which resulted in glutamate release. The amount of released glutamate was decreased in cells with suppressed exocytosis and after pharmacological block of hemichannels. The data demonstrate that SGCs of the trigeminal ganglion release glutamate in a Ca(2+)-dependent manner.
有人提出,谷氨酸在感觉神经节中充当神经元与卫星神经胶质细胞(SGCs)之间的介质,且SGCs会释放谷氨酸。我们采用一种新方法,研究了来自小鼠三叉神经节的SGCs释放谷氨酸的情况。将带有附着SGCs的感觉神经元从野生型和转基因小鼠中酶解分离出来,其中转基因小鼠的神经胶质细胞中囊泡胞吐作用受到抑制。通过微荧光测定法检测细胞外谷氨酸。在用对光不稳定的Ca(2+)螯合剂加载细胞后,通过紫外线脉冲提高SGCs中的细胞内Ca(2+)浓度,这导致谷氨酸释放。在胞吐作用受到抑制的细胞以及半通道药理学阻断后,释放的谷氨酸量减少。数据表明,三叉神经节的SGCs以Ca(2+)依赖的方式释放谷氨酸。