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Year : 1976  |  Volume : 24  |  Issue : 1  |  Page : 22-25

Retinal abnormalities in albino rats

King George's Medical College, Lucknow, India

Correspondence Address:
K K Bisaria
King George's Medical College, Lucknow
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Source of Support: None, Conflict of Interest: None

PMID: 1031380

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How to cite this article:
Bisaria K K. Retinal abnormalities in albino rats. Indian J Ophthalmol 1976;24:22-5

How to cite this URL:
Bisaria K K. Retinal abnormalities in albino rats. Indian J Ophthalmol [serial online] 1976 [cited 2023 Dec 10];24:22-5. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1976/24/1/22/31104

Hall[3] described developmental anomalies in the retina after trauma. Bourne, Campbell and Tansley[1] demonstrated hereditary degeneration of the retina in the rats. The present work is the collection of accidental findings of retinal abnormalities during the course of some other investigations in the albino rats, which are very rare.

  Materials and Methods Top

In total 40 adult albino rats from different sources weighing 120-130 gms and 17-20 days old of either sexes were taken for a study. They were exsanguated under ether anaesthesia by cutting the carotid lartery. All the enucleated eyeballs were fixed in Bouin's fluid and paraffin sections were cut at 5 microns. The sections were stained with haematoxylin and eosin.

  Observations Top

Normal retinae mere found in 56 eyeballs of 28 rats. It showed from without inward layer of rods, outer nuclear layer, outer fibre layer. inner nuclear layer, inner fibre layer, ganglionic layer and optic nerve fibre layer [Figure - 1][Figure - 2]. The pigment epithelium as is natural in albino rats could not be clearly seen on account of absence of pigments.

In 10 retinae of the 5 male rats the rod layers were completely absent.[Figure - 3]. In 4 retinae of 2 female rats there was non-uniformity of the rod layer. At places this layer showed collection of network of glial fibres [Figure - 4]. In 2 retinae of a female rat there was collection of glial tissue in the rod layer with a portion of it invaginating into the outer nuclear layer [Figure - 5]. In 2 retinae of a male rat there mas disintegra­tion of rod layer with number of vacuoles in it and in the optic nerve fibre layer [Figure - 6]. In 2 retinae of a female rat the retinal blood vessels were markedly congested [Figure - 7]. In 4 retinae of 2 male rats retinal fibre bands were seen crossing all the layers of retinae from the region of choroid to the stratum opticum [Figure - 8].

  Discussion Top

The causal mechanism of production of ocular anomalies in the mammals is obscure. Gruenwald[2]- while reviewing the literature des­cribed that there are various agents which produce developmental ocular anomalies.

It has been an interesting feature that out of 80 eyeballs of both sexes of adult rats 24 retinae showed abnormalities like complete absence of rod layer, irregular thickness of rod layer on account of glial tissue collection, in­vagination of rod layer into the outer nuclear layer, vacuoles in the retinal lavers, congestion of retinal blood vessels and the presence of retinal fibre bands across the all layers of retinae. The absence of rod layer in the retina is probably on account of activity of phagocytes on this disintegrated layer. It is observed in this work that in majority the rod layer was the site of defects.

  Summary Top

A total number of 40 adult albino rats were taken for a study. The retinal abnormalities in­cluded defects like absence of rod layers, non­uniformity of rod layer, abnormal collection of glial tissue in the rod layer and invagination of rod layer in the outer nuclear layer, vacuoles in rod and optic nerve fibre layer, unusual marked congestion of retinal blood vessels and retinal fibre bands.

  References Top

Bourne, M.C., Campbell, D.A. and Tansley, K. Hereditary, 1938, Brit. J. Ophthal., 22, 613.  Back to cited text no. 1
Gruenwald, P., 1947 , Arch. Path., 44, 398, 495, 648.  Back to cited text no. 2
Hall, E.K., 1953. Anat. Rec., 116, 383.  Back to cited text no. 3


  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8]


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