Modulation of metabotropic glutamate receptors fails to prevent the loss of adult rat retinal ganglion cells following axotomy or N-methyl-D-aspartate lesion in vivo

Both optic nerve (ON) transection and intraocular injection of N-methyl-D-a spartate (NMDA) are established lesion models to cause death of retinal gan glion cells (RGCs) in the adult rat. Excitotoxic effects via glutamate rece ptors resulting in secondary neuronal death are discussed as possible initi ators in both types of RGC damage. We examined whether modulating glutamate rgic transmission through metabotropic glutamate receptors rescues RGCs fro m lesion-induced degeneration in vivo. Unexpectedly, repeated intraocular i njection of four different agonists/antagonists on the various subtypes of mGluRs did not decrease retinal damage in both lesion paradigms as revealed by measurement of visual performance and RGC survival. We conclude that ac tivation/inactivation of retinal mGluRs does not play an important role for the initiation and execution of secondary RGC loss after ON transection an d NMDA lesion in the adult rat. (C) 2001 Elsevier Science Ltd. All rights r eserved.