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Plasma-induced changes in the physiology of mammalian retinal glial cells: Role of glutamate
Authors
Amos
Arriza
+66 more
Attwell
Baba
Benveniste
Boss
Boss
Bruno
Bushell
Cai
Casabona
Choi
Cholewinski
Estin
Fairman
Forsythe
Fosse
Gegelashvili
Genazzani
Gilbert
Griffiths
Hayashi
Isaacson
Ito
Izumi
Jane
Kanai
Kawabata
Keinanen
Kemp
Levi
Lindsay
Longuemare
Manahan-Vaughan
Masu
Mennerick
Miller
Miller
Nicholls
Nicoletti
Ogata
Ottersen
Patneau
Petralia
Pin
Pines
Porter
Prezeau
Rothstein
Rutledge
Schoepp
Stein
Storck
Swanson
Szatkowski
Tanabe
Tanaka
Testa
Velasco
Volterra
Winder
Winder
Winder
Ye
Ye
Ye
Zerangue
Zorumski
Publication date
1 February 1999
Publisher
'Wiley'
Doi
Abstract
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 MÜller cells, the principal glia of the retina. To monitor the function of MÜller cells in situ, we recorded electroretinograms from isolated retinas. We found that plasma activates an electrogenic glutamate transporter and inhibits inward-rectifying K + 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 MÜller cells responding to light-evoked changes in the extracellular potassium concentration ([K + ] O ). Taken together, our observations indicate that a leakage of serum into the retina compromises the regulation of [K + ] O by MÜller cells; however, when plasma enters the retina at sites of a breakdown in the blood-retinal barrier, these glia can maintain K + homeostasis while reducing the potentially neurotoxic levels of glutamate. GLIA 25:205–215, 1999. © 1999 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/35021/1/1_ftp.pd
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