Plasma-induced changes in the physiology of mammalian retinal glial cells: Role of glutamate

✍ Scribed by Shunji Kusaka; Natalia V. Kapousta-Bruneau; Donald G. Puro

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 151 KB
• Volume: 25
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/(sici)1098-1136(19990201)25:3<205::aid-glia1>3.0.co;2-s

✦ Synopsis

Plasma can leak into the nervous system when the vascular endothelial barrier is compromised. Although this occurs commonly, little is known about the effects of plasma on the function of cells in the central nervous system. In this study, we focused on the responses of glial cells, which, because they ensheathe the blood vessels, are the first cells exposed to leaking plasma. We used the perforated-patch configuration of the patch-clamp technique to assess the effects of plasma on freshly dissociated bovine and human Mu ¨ller cells, the principal glia of the retina. To monitor the function of Mu ¨ller cells in situ, we recorded electroretinograms from isolated retinas. We found that plasma activates an electrogenic glutamate transporter and inhibits inward-rectifying K ϩ channels, as well as a transient outward current. Glutamate, a normal constituent of the blood, mimicked these effects. Unlike our recent findings with serum, which contains molecules generated by the clotting process, plasma neither activated a nonspecific cation conductance nor inhibited the slow P III component of the electroretinogram, which is generated by Mu ¨ller cells responding to light-evoked changes in the extracellular potassium concentration ([K ϩ ] O ). Taken together, our observations indicate that a leakage of serum into the retina compromises the regulation of [K ϩ ] O by Mu ¨ller cells; however, when plasma enters the retina at sites of a breakdown in the blood-retinal barrier, these glia can maintain K ϩ homeostasis while reducing the potentially neurotoxic levels of glutamate. GLIA 25:205-215, 1999.