advertisement
The present study was initiated to investigate neuronal degeneration, microglial reactivity and possible roles of NO in the lateral geniculate nucleus (LGN) of glaucomatous rats. An experimental one-eye glaucoma model was created by cauterization of the limbal-derived veins. Neuronal cell viability was studied by immunostaining with antibody against neuronal nuclei. Changes of expressions of nitric oxide synthase I (NOS I), NOS II, ED 1, OX6 and OX42 in the LGN were studied by immunohistochemistry. NADPH-d histochemistry was also employed. In the experimental glaucomatous rats, the number of NeuN labelled neurons was significantly decreased in both the ipsi- and contra-lateral sides of the ventral LGN (vLGN) but not the dorsal LGN (dLGN) at one month post-operation and beyond. Expressions of NOS I and NADPH-d were notably increased from one week post-operation in the ipsilateral vLGN. In the contralateral side of the vLGN, however, this change was only observed from one month post-operation. No NOS II immunoreaction was observed in LGN of both the normal control and glaucomatous rats. Increased microglial reactivity as indicated by OX-42 immunoreactivity was first observed in both sides of the LGN at one week post-operation, and this was most significant especially at one and two months post-operation. The present results suggest that NO and microglial cells may play some important roles in the pathologic processes of neuronal degeneration in the LGN of glaucomatous rats.
Dr. S.S.-W. Tay, Department of Anatomy, Faculty of Medicine, National University of Singapore, 4 Medical Drive, Singapore 117597, Singapore
1.3 Pathogenesis (Part of: 1 General aspects)