Chloride enters glial cells and photoreceptors in response to light stimulation in the retina of the honey bee drone

✍ Scribed by Jonathan A. Coles; Dr. Richard K. Orkand; Dr. Carol L. Yamate

• Publisher: John Wiley and Sons
• Year: 1989
• Tongue: English
• Weight: 1001 KB
• Volume: 2
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/glia.440020502

✦ Synopsis

Double-barrelled ion-selective microelectrodes were used to measure free [Cl-] in photoreceptors, extracellular space, and glial cells in superfused slices of drone retina. Tests indicated that with normal superfusate the intracellular electrode signal was due essentially to C1-and not to some other interfering anion. The results indicate that C1-is more concentrated in both photoreceptors and glial cells than would be predicted for a passive electrochemical distribution. When the photoreceptors were stimulated by a standard train of 20 ms flashes, 11s for 90 s, their intracellular free [Cl-I (Cli) rose by 8 +-1 mM. At the end of stimulation Cli usually continued to rise for up to a further 2 min and then returned toward the baseline over about 10 min. During light stimulation Cli in the glia rose. The magnitude of the increase was 5.1 2 0.4 mM, about half the increase in Ki. In some extracellular recording sites, light stimulation caused [Cl-1 to increase and in others to decrease. The mean change was -0.7 mM, SD 6.5 mM. The C1-that entered the photoreceptors and the glia was presumably made available by the shrinking of the extracellular space. When the cells were depolarized by increasing [K+] in the superfusate from 7.5 mM to 18 mh4, Cli increased. The half-time of the change in Cli was longer than the half-time of the depolarization by 10-30 s in the glia and 50-250s in the photoreceptors. During superfusion with 0 C1-Ringer's solution, the light-induced rise in extracellular [K+] was greater by a factor of 1.4-2.7, and the clearance after the end of the stimulation was slower. The rate of increase in glial during light stimulation fell; the rate of increase of glial Ki caused by superfusion with raised [K+l (in the absence of C1-) fell more. We conclude that when extracellular [K+] is increased, entry of C1-into the glia is necessary for part, but not all, of the net uptake of K+. During light stimulation, the observed movement of Cl-into glia contributes to homeostasis of extracellular [K+l, and the cell swelling associated with movement of C1into both glia and photoreceptors contributes to homeostasis of extracellular "a' ].