Nitric oxide, microglial activities and neuronal cell death in the lateral geniculate nucleus of glaucomatous rats.

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 1 month post-operation and beyond. Expressions of NOS I and NADPH-d were notably increased from 1 week post-operation in the ipsilateral vLGN. In the contralateral side of the vLGN, however, this change was only observed from 1 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 1 week post-operation, and this was most significant especially at 1 and 2 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.