An Investigation of the Retinal Layers in an Experimental Model of Multiple Sclerosis; a Histopathological and Immunohistochemical Study

Background: Animal model of multiple sclerosis is a demyelinating and inflammatory disorder of central nervous system and eye. Histological evaluation in eyes in experimental autoimmune encephalomyelitis (EAE) models demonstrated evidence of retinal atrophy and inflammation in late stage of disease. Deciphering the relationships between the retinal atrophy and proliferation on retinal layers may help us in understanding the factors that drive atrophy and proliferation in multiple sclerosis.

Aims: The aim of the present study was to determine alterations in thickness of retina and its sub-layers in MS induced mice model in comparison with control group.

Study Design: Experimental study.

Methodology: EAE was induced in female C57BL/6 mice using Hooke kits. Animals were scored for clinical signs of the disease according to 10-point EAE scoring system. At 35th day after immunization, mice (n=15/group) were deeply anesthetized and eyes were removed.

Morphometric study of proliferation in retinal sub-layers were assessed by Hematoxilen and Eosin staining and expression of Ki67. The proliferating marker was performed by Ki67analyzing kit. All measurement obtained by Motic image analyzer software 2 and analyzed spss 18, respectively.

Results: Here we reported that retinal thickness in MS group including total retinal layer, especially photoreceptor layer, ganglion cell layer and neural layer reduced in comparison to control group (p< 0.001). In Ms Group proliferation rate is also decreased in comparison to control group (0.05).

Conclusion: Our results show that ki67 expression, as an indication of proliferation, decreased in retinal layers in MS group. Furthermore, our data revealed that retinal thickness also decreased in MS group.