Electrophysiological properties of rat retinal Muller (glial) cells in postnatally developing and in pathologically altered retinae

被引:38
作者
Felmy, F
Pannicke, T
Richt, JA
Reichenbach, A
Guenther, E
机构
[1] Univ Leipzig, Paul Flechsig Inst Hirnforsch, D-04109 Leipzig, Germany
[2] Univ Tubingen, Augenklin Abt 2, Forschungsstelle Expt Ophthalmol, Lab Zellphysiol & Mol Biol, D-7400 Tubingen, Germany
[3] Univ Giessen, Inst Virol, D-6300 Giessen, Germany
关键词
patch clamp; K+ channels; development; RCS rat; borna disease;
D O I
10.1002/glia.1053
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Retinal glial Muller 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 Muller 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 Muller 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 M Omega to less than 50 M Omega was accompanied by a shift of the zero current potential from about -20 mV to -80 mV, similar as earlier observed in developing rabbit Muller 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 Muller cells. Thus, rat Muller cells fail to change their basic membrane properties in two different models of retinal pathology. This is in contrast to human and rabbit Muller cells, which have been shown to undergo dramatic changes of their membrane physiology in response to retinal diseases and injuries. GLIA 34: 190-199, 2001. (C) 2001 Wiley-Liss, Inc.
引用
收藏
页码:190 / 199
页数:10
相关论文
共 50 条
[1]  
BIGNAMI A, 1979, EXP EYE RES, V28, P63
[2]   MEMBRANE-POTENTIALS AND SODIUM-CHANNELS - HYPOTHESES FOR GROWTH-REGULATION AND CANCER FORMATION BASED ON CHANGES IN SODIUM-CHANNELS AND GAP-JUNCTIONS [J].
BINGGELI, R ;
WEINSTEIN, RC .
JOURNAL OF THEORETICAL BIOLOGY, 1986, 123 (04) :377-401
[3]   Properties of human glial cells associated with epileptic seizure foci [J].
Bordey, A ;
Sontheimer, H .
EPILEPSY RESEARCH, 1998, 32 (1-2) :286-303
[4]   Electrophysiological properties of human astrocytic tumor cells in situ: Enigma of spiking glial cells [J].
Bordey, A ;
Sontheimer, H .
JOURNAL OF NEUROPHYSIOLOGY, 1998, 79 (05) :2782-2793
[5]  
Bringmann A, 2000, CURR EYE RES, V20, P420, DOI 10.1076/0271-3683(200005)20:5
[6]  
1-1
[7]  
FT420
[8]   Expression of potassium channels during postnatal differentiation of rabbit Muller glial cells [J].
Bringmann, A ;
Biedermann, B ;
Reichenbach, A .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1999, 11 (08) :2883-2896
[9]  
Bringmann A, 2000, GLIA, V29, P35, DOI 10.1002/(SICI)1098-1136(20000101)29:1<35::AID-GLIA4>3.0.CO
[10]  
2-A