The developmental expression of K+ channels in retinal glial cells is associated with a decrease of osmotic cell swelling.
A major function of glial cells is the control of osmotic and ionic homeostasis, mediated by K+ and water movements predominantly through inwardly rectifying K+ (Kir) and aquaporin water channels. It has been suggested that K+ currents through Kir channels are implicated in the regulation of glial cell volume. Here, we investigated whether the developmental increase in Kir channel expression in Müller glial cells of the rat retina is associated with an alteration of cell volume regulation under anisoosmotic conditions. Around the time of eye opening at postnatal day (P) 15, developing retinal glial cells fully alter the profile of their membrane conductances, from a current pattern with prominent fast transient K+ and Na+ currents to a pattern of noninactivating currents through Kir and delayed rectifier K+ channels. Concomitantly, aquaporins-1 and -4 are expressed in the developing retina. This is accompanied by a conspicuous alteration of the swelling characteristics of cells; somata of immature glial cells in early postnatal retinas (P5-P15) swell under hypotonic stress but no swelling is inducible in mature cells at P18 and thereafter. However, glial cells at all developmental stages swell when their Kir channels are blocked by Ba2+. The postnatal maturation of Kir channel currents and volume regulation in retinal glial cells is delayed by visual deprivation. The data suggest that Kir channels are crucially involved in osmotic volume homeostasis of mature glial cells, and that the absence of Kir channels in immature cells is a major cause of their insufficient volume regulation.
Wurm
Antje
A
Paul Flechsig Institute of Brain Research, University of Leipzig Medical Faculty, Leipzig, Germany.
Pannicke
Thomas
T
Iandiev
Ianors
I
Wiedemann
Peter
P
Reichenbach
Andreas
A
Bringmann
Andreas
A
D000818:Animals; D000831:Animals, Newborn; D020346:Aquaporins / Q000378:metabolism; D001464:Barium / Q000494:pharmacology; D002352:Carrier Proteins / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D002463:Cell Membrane Permeability / Q000187:drug effects / Q000502:physiology*; D048429:Cell Size / Q000187:drug effects; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism*; D009924:Organ Culture Techniques; D009997:Osmotic Pressure / Q000187:drug effects; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024661:Potassium Channels, Inwardly Rectifying / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D020318:Rats, Long-Evans; D012160:Retina / Q000166:cytology / Q000254:growth & development* / Q000378:metabolism*; D015222:Sodium Channels / Q000378:metabolism; D013312:Stress, Physiological / Q000378:metabolism / Q000503:physiopathology; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology*; D000098854:Kcnj10 Channel
C020932:11-cis-retinal-binding protein; D020346:Aquaporins; D002352:Carrier Proteins; D000098854:Kcnj10 Channel; D026902:Potassium Channel Blockers; D024661:Potassium Channels, Inwardly Rectifying; D015222:Sodium Channels; D001464:Barium; D005974:Glutamate-Ammonia Ligase