Antigens associated with specific retinal cells are affected by ischaemia caused by raised intraocular pressure: effect of glutamate antagonists

Neurochem Int. 1996 Sep;29(3):263-70. doi: 10.1016/0197-0186(96)00005-8.


Raising the rat's intraocular pressure above the systolic blood pressure for 60 min followed by a reperfusion of 7-10 days caused an ischaemic insult to the retina. The b-wave of the electroretinogram was abolished and the retinal thickness was much reduced, the greatest influence being associated with the inner retinal layers. No obvious histological damage was apparent at the light microscopy level. Immunocytochemistry, however, revealed a clear change in the nature of certain antigens associated with specific cell-types. Thy-1 antigen located to ganglion cell membranes was much reduced, suggesting that the ganglion cells are affected by ischaemia. Calretinin-immunoreactivity associated with amacrine cells is drastically reduced by ischaemia. In contrast, Ret-P1, located to the outer segments of the photoreceptors is unaffected by ischaemia. Ischaemia also caused GFAP-immunoreactivity to be expressed in the Müller cells, which is normally only associated with astrocytes in the ganglion/nerve fibre layer. Injection of a mixture of CNQX and MK-801, kainate and NMDA receptor antagonists, respectively, into the eye just before ischaemia failed to reverse the changes induced by the insult. However, analysis 3 days after reperfusion revealed that when the ischaemic insult was reduced to 45, rather than 60 min, the changes in the calretinin-immunoreactivity were reversed. The results show that immunocytochemistry provides a powerful way of following biochemical changes associated with specific cell types caused by ischaemia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens / metabolism*
  • Calbindin 2
  • Electroretinography
  • Excitatory Amino Acid Antagonists / pharmacology*
  • Eye Proteins / metabolism
  • Glial Fibrillary Acidic Protein / metabolism
  • Glutamic Acid / physiology
  • Immunohistochemistry
  • Intraocular Pressure / physiology*
  • Ischemia / physiopathology*
  • Rats
  • Rats, Wistar
  • Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
  • Reperfusion Injury / metabolism
  • Retina / cytology
  • Retina / metabolism*
  • Retinal Vessels / physiology*
  • S100 Calcium Binding Protein G / metabolism
  • Thy-1 Antigens / metabolism


  • Antigens
  • Calb2 protein, rat
  • Calbindin 2
  • Excitatory Amino Acid Antagonists
  • Eye Proteins
  • Glial Fibrillary Acidic Protein
  • Receptors, N-Methyl-D-Aspartate
  • S100 Calcium Binding Protein G
  • Thy-1 Antigens
  • Glutamic Acid