%0 Journal Article
%T Correlations between ERG, OCT, and Anatomical Findings in the rd10 Mouse
%A Sarah Rˋsch
%A Sandra Johnen
%A Frank M邦ller
%A Christiane Pfarrer
%A Peter Walter
%J Journal of Ophthalmology
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/874751
%X Background. To evaluate the correlation between ERG, OCT, and microscopic findings in the rd10 mouse. Methods. C57BL/6J wild type mice and rd10 mice were compared at the age of 2, 3, 5, 7, 9, 12, 24, and 48 weeks (each age group ) using full-field electroretinography (ERG), spectral domain Optical Coherence Tomography (sd-OCT), fluorescein angiography (FA), Hematoxylin & Eosin histology (HE), and immunohistology (IH). Results. While in wild type mice, the amplitude of a- and b-wave increased with light intensity and with the age of the animals, the rd10 mice showed extinction of the ERG beginning with the age of 5 weeks. In OCT recordings, the thickness of the retina decreased up to 9 weeks of age, mainly based on the degradation of the outer nuclear layer (ONL). Afterwards, the ONL was no longer visible in the OCT. HE staining and immunohistological findings confirmed the in vivo data. Conclusion. ERG and OCT are useful methods to evaluate the retinal function and structure in vivo. The retinal changes seen in the OCT closely match those observed in histological staining. 1. Introduction Hereditary dystrophies of the retina, such as Retinitis pigmentosa (RP), are considerable causes of blindness in humans [1]. Research efforts concerning these currently not treatable diseases are focused on the genetic background, the mechanisms of degeneration, and possible treatment strategies [2]. Animal models in rodents, for example, the retinal degeneration rd1 and rd10 mice, are well characterized and described [3每9]. In rd1 and rd10 mice, missense point mutations in the gene encoding for the 汕-subunit of rod cGMP phosphodiesterase type 6 (汕PDE) result in the described disease pattern [3每9]. The gene mutation leads to the degeneration of first rods and then consecutively cones with a central to peripheral gradient [9]. The fact that in both animal models firstly rods and secondly cones degenerate, which is comparable to RP [3每9], seems to be caused by missing diffusible factors normally secreted by the rods [10]. This kind of retinal degeneration is concomitant with a pronounced reduction in the thickness of the outer nuclear layer (ONL) [3每9]. The thickness of the inner retinal layers remains nearly unaffected [3每9]. The retinal development in the rd1 and rd10 mice is comparable to normal mice up to postnatal day 8 (P8) [2]. However, while in rd1 mice, the degeneration becomes apparent at P11, in rd10 mice, the degeneration starts at P16 and the peak of photoreceptor degeneration is reached at P25 [9]. By P60, no photoreceptors are left [9]. Because of the
%U http://www.hindawi.com/journals/joph/2014/874751/