ABSTRACT
Differential, or selective, vulnerability of retinal neurons suggests multiple potential targets for cell- or pharmacological-based neuroprotective interventions. Despite the promise of neurotrophin-based therapies, targeted delivery of proteins to specific neurons is difficult to achieve. Glutamate receptor overactivation that results from ischemic injury, and perhaps from chronic neurodegenerative disease as well, is enhanced during reperfusion. The continued availability of adequate trophic support appears to be crucial not only for the development of nerve cells and their interconnecting circuitry, but also for the maintenance of neurons and their synapses in the adult. The initial stage in the development of functional retinal circuitry is the differentiation of retinal ganglion cells. Excitatory neurotransmission in the central nervous system, including the retina, is accomplished primarily by the amino acid glutamate. The mammalian retina comprises a rich, heterogeneous mosaic of neuronal morphological phenotypes intermeshed in an intricate pattern of synaptic connectivity.
