Abstract
Glutamate is an important amino acid, metabolite and excitatory neurotransmitter, which is found in its free form in the extracellular spaces of the central nervous system (CNS). More than half of all synapses in CNS release glutamate. It is the main neurotransmitter driving the light responses in the retina. All types of photoreceptors, bipolar, ganglion and one type of glycinergic amacrine cells express specific subtypes of vesicular glutamate transporters and are the main source of endogenous glutamate in retina, besides Müller glia that are responsible for glutamate homeostasis, release and reuptake. Reduced or excessive extracellular glutamate was detected in the synaptic clefts of several naturally occurring or transgenic eye disease models, in which network rewiring and altered functions were observed. These led to the hypothesis that glutamate is one of the extrinsic signals for visual pathway development. This minireview examines experimental evidences supporting, or refuting, the influence of glutamate on prenatal and postnatal retinal development.
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