Electrophysiological properties of rat retinal Müller (glial) cells in postnatally developing and in pathologically altered retinae.
Retinal glial Müller cells are characterized by dominant K(+) conductances. The cells may undergo changes of their membrane currents during ontogeny and gliosis as described in rabbit and man. Although the rat retina is often used in physiological experiments, the electrophysiology of rat Müller cells is less well studied. The aim of the present study was to characterize their membrane currents in postnatal development and in two models of retinal degeneration. Freshly isolated cells were subjected to whole-cell patch clamp recordings. During the first 4 weeks after birth of rats, their Müller cells displayed an increase in all membrane currents, particularly in the inward currents elicited at hyperpolarizing potentials. The decrease of the membrane resistance from more than 760 MOmega to less than 50 MOmega was accompanied by a shift of the zero current potential from about -20 mV to -80 mV, similar as earlier observed in developing rabbit Müller cells. These developmental changes were found in pigmented Brown Norway rats as well as in rats with inherited retinal dystrophy (RCS rats). Moreover, an infection of Lewis rats with the Borna disease virus caused substantial neuroretinal degeneration but did not result in a strong reduction of inward currents and of the zero current potential of the Müller cells. Thus, rat Müller cells fail to change their basic membrane properties in two different models of retinal pathology. This is in contrast to human and rabbit Müller cells, which have been shown to undergo dramatic changes of their membrane physiology in response to retinal diseases and injuries.
Felmy
F
F
Forschungsstelle für Experimentelle Ophthalmologie, Universitäts-Augenklinik Abt. II, Labor für Zellphysiologie und Molekularbiologie, Tübingen, Germany.
Pannicke
T
T
Richt
J A
JA
Reichenbach
A
A
Guenther
E
E
D000818:Animals; D001891:Borna disease virus / Q000502:physiology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D008564:Membrane Potentials / Q000502:physiology*; D009457:Neuroglia / Q000473:pathology / Q000502:physiology*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D011917:Rats, Inbred Lew; D011922:Rats, Mutant Strains; D012160:Retina / Q000473:pathology / Q000503:physiopathology*; D012162:Retinal Degeneration / Q000473:pathology / Q000503:physiopathology*
D015221:Potassium Channels