Department of Ophthalmology, Ruijin Hospital Affiliated Medical School, Shanghai Jiaotong University, 197 Ruijin Er Road, Shanghai 200025, China.
Shanghai Key Laboratory for Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopaedics, Ruijin Hospital Affiliated Medical School, Shanghai Jiaotong University, 197 Ruijin Er Road, Shanghai 200025, China.
Biomed Res Int. 2018 Aug 29;2018:2749257. doi: 10.1155/2018/2749257. eCollection 2018.
The vitreousness of glaucoma subjects contains elevated glutamate, and excessive extracellular glutamate is toxic to retinal neurons. Therefore, glutamate clearance is potentially impaired in the retina of glaucoma subjects. Müller cells play an important role in maintaining low extracellular levels of neurotransmitters, such as glutamate. A better understanding of the cross-talk between adenosine and glutamate may provide a better characterization of the regulatory network in Müller cells. Here, Müller cells were purified from the rat retina on postnatal day 5 using the papain digestion method. Application of increasing concentrations of glutamate (0-20 mmol/L) caused a dose-dependent decrease in the expression levels of Kir4.1, Kir2.1, GLAST, and GS. Exogenous adenosine regulated Kir channels and subsequently promoted GLAST and GS expression levels in Müller cells under exogenous glutamate stimulation. These effects were partly dependent on adenosine receptors.
青光眼患者的玻璃体中含有升高的谷氨酸,细胞外过多的谷氨酸对视网膜神经元有毒性。因此,青光眼患者的视网膜中谷氨酸的清除可能受损。Müller 细胞在维持神经递质(如谷氨酸)的细胞外低水平方面发挥着重要作用。更好地了解腺苷和谷氨酸之间的串扰可能会更好地描述 Müller 细胞中的调控网络。在这里,使用木瓜蛋白酶消化法从小鼠视网膜中分离出生后 5 天的 Müller 细胞。应用浓度逐渐增加的谷氨酸(0-20mmol/L)会导致 Kir4.1、Kir2.1、GLAST 和 GS 的表达水平呈剂量依赖性下降。外源性腺苷调节 Kir 通道,随后在外源谷氨酸刺激下促进 Müller 细胞中 GLAST 和 GS 的表达水平。这些作用部分依赖于腺苷受体。