Degenerative alterations in the visual pathway after NMDA-induced retinal damage in mice

Abstract

In the present study, intravitreal injection of N-methyl- d-aspartate (NMDA) into the left eye induced retinal damage (decreases in the number of retinal ganglion cells) at 1 day after the injection. At 7 days after the injection, atrophy of the optic tract was observed on the contralateral side, but not on the ipsilateral side. Number of neuronal nuclear specific protein (NeuN)-immunostained neurons were decreased in the contralateral dorsal LGN (dLGN) and contralateral ventral LGN-lateral (vLGN-l) at 90 and 180 days, respectively, after the injection. Furthermore, expressions of glial fibrillary acid protein (GFAP) were increased in the contralateral dLGN and contralateral vLGN-l at 7 and 30 days, respectively, and those of brain-derived neurotrophic factor (BDNF) were increased in the contralateral dLGN at 30 and 90 days and in the contralateral vLGN-l at 7 and 30 days. All NeuN-positive neuronal cells exhibited BDNF, whereas only some GFAP-positive astroglial cells exhibited BDNF. However, the contralateral ventral LGN-medial (vLGN-m) and ipsilateral LGN displayed no significant differences related to NeuN, GFAP, or BDNF immunohistochemistry. Taken together, these results indicate that time-dependent alterations occurred after the NMDA injection along the retinogeniculate pathway (from retina to LGN), and that the degree of damage in the LGN was region-dependent. In addition, the increased activated astroglial cells and expressions of BDNF in the damaged regions may play some roles in the cell-survival process of the LGN.