Ganglion cell responses to retinal light stimulation in the absence of photoreceptor outer segments from retinal degenerate rodents

被引:19
作者
An, GJ
Asayama, N
Humayun, MS
Weiland, J
Cao, JT
Kim, SY
Grebe, RR
de Juan, E
Sadda, SR
机构
[1] Johns Hopkins Univ, Sch Med, Wilmer Ophthalmol Inst, Baltimore, MD 21287 USA
[2] Univ So Calif, Keck Sch Med, Doheny Eye Inst, Retina Inst, Los Angeles, CA USA
关键词
retinal degeneration; rodents; photoreceptor outer segments; retinal surface recordings; ganglion cell responses;
D O I
10.1076/ceyr.24.1.26.5432
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Purpose. To determine whether a severely degenerated retina without photoreceptor outer segments and a non-recordable electroretinogram (ERG) can still show retinal ganglion cell (RGC) responses to retinal light stimulation. Methods. The authors measured ERGs and retinal surface RGC responses from six week old rd mice and three month old homozygous S334ter line3 rats. Animal eyes were also studied by light microscopy, transmission electron microscopy, and immunohistochemistry (rats). Results. The corneal ERGs were non-recordable and no photoreceptor outer segments were found in either retinal degeneration model. A few cell bodies (without outer segments) that were immunoreactive for cone opsin and rhodopsin were found in the outer nuclear layer of the rats. Light-driven ON-RGC responses, however, were recordable from six week old rd mice. In addition, light-driven ON and OFF-RGC responses were recordable from three month old homozygous S334ter line 3 rats. Conclusions. This study suggests that despite the apparent absence of photoreceptor outer segments and a nonrecordable ERG, ganglion cell responses to retinal light stimulation may remain preserved in some severe retinal degenerate transgenic rodents.
引用
收藏
页码:26 / 32
页数:7
相关论文
共 29 条
[1]   ANTI-RHODOPSIN MONOCLONAL-ANTIBODIES OF DEFINED SPECIFICITY - CHARACTERIZATION AND APPLICATION [J].
ADAMUS, G ;
ZAM, ZS ;
ARENDT, A ;
PALCZEWSKI, K ;
MCDOWELL, JH ;
HARGRAVE, PA .
VISION RESEARCH, 1991, 31 (01) :17-31
[2]  
BERSON EL, 1993, INVEST OPHTH VIS SCI, V34, P1659
[3]   RETINAL DEGENERATION IN THE RD MOUSE IS CAUSED BY A DEFECT IN THE BETA-SUBUNIT OF ROD CGMP-PHOSPHODIESTERASE [J].
BOWES, C ;
LI, TS ;
DANCIGER, M ;
BAXTER, LC ;
APPLEBURY, ML ;
FARBER, DB .
NATURE, 1990, 347 (6294) :677-680
[4]  
CARTERDAWSON LD, 1978, INVEST OPHTH VIS SCI, V17, P489
[5]   STUDIES OF VISUAL FUNCTION AND ITS DECAY IN MICE WITH HEREDITARY RETINAL DEGENERATION [J].
DRAGER, UC ;
HUBEL, DH .
JOURNAL OF COMPARATIVE NEUROLOGY, 1978, 180 (01) :85-114
[6]   3 CONE MECHANISMS IN THE PRIMATE ELECTRORETINOGRAM - 2 WITH, ONE WITHOUT OFF-CENTER BIPOLAR RESPONSES [J].
EVERS, HU ;
GOURAS, P .
VISION RESEARCH, 1986, 26 (02) :245-254
[7]   CIRCADIAN PHOTORECEPTION IN THE RETINALLY DEGENERATE MOUSE (RD/RD) [J].
FOSTER, RG ;
PROVENCIO, I ;
HUDSON, D ;
FISKE, S ;
DEGRIP, W ;
MENAKER, M .
JOURNAL OF COMPARATIVE PHYSIOLOGY A-SENSORY NEURAL AND BEHAVIORAL PHYSIOLOGY, 1991, 169 (01) :39-50
[8]   ULTRASTRUCTURAL LOCALIZATION OF RHODOPSIN IN VERTEBRATE RETINA [J].
JAN, LY ;
REVEL, JP .
JOURNAL OF CELL BIOLOGY, 1974, 62 (02) :257-273
[9]  
KARLI P, 1954, ARCH SCI PHYSIOL, V8, P305
[10]  
KARPE G, 1949, T OPHTHAL SOC UK, V69, P237