Retina glutamate

Brandstatter, I. H. Glutamate receptors in the retina the molecular substrate for visual signal processing. Curr. Eye Res. 25 327-331, 2002. 

Mort, D., Marcaggi, P Grant, J., and Attwell, D. (2001) Effect of acute exposure to ammonia on glutamate transport in glial cells isolated from the salamander retina../. Neurophysiol. 86, 836-844. 

Spiridon, M., Kamm, D Billups, B., Mobbs, P, and Attwell, D. (1998) Modulation by zinc of the glutamate transporters in glial cells and cones isolated from the tiger salamander retina../. Physiol. (Lond). 506, 363-376. 

P. Louzada-Junior, J. J. Dias, W. F. Santos, J. J. Lachat, H. F. Bradford, and J. Coutinho-Netto. Glutamate release in experimental ischaemia of the retina An approach using microdialysis. J. Neurochem. 59 358-363 (1992). 

Physiological studies have identified both post- and presynaptic roles for ionotropic kainate receptors. Kainate receptors contribute to excitatory post-synaptic currents in many regions of the CNS including hippocampus, cortex, spinal cord and retina. In some cases, postsynaptic kainate receptors are codistributed with AMPA and NMDA receptors, but there are also synapses where transmission is mediated exclusively by postsynaptic kainate receptors for example, in the retina at connections made by cones onto off bipolar cells. Extrasynaptically located postsynaptic kainate receptors are most likely activated by spill-over glutamate (Eder et al. 2003). Modulation of transmitter release by presynaptic kainate receptors can occur at both excitatory and inhibitory synapses. The depolarization of nerve terminals by current flow through ionotropic kainate receptors appears sufficient to account for most examples of presynaptic regulation however, a number of studies have provided evidence for metabotropic effects on transmitter release that can be initiated by activation of kainate receptors. The hyperexcitability evoked by locally applied kainate, which is quite effectively reduced by endocannabinoids, is probably mediated preferentially via an activation of postsynaptic kainate receptors (Marsicano et al. 2003). 

The excitatory transmitter released from these cells is, in most instances, glutamate. Local circuit neurons are typically smaller than projection neurons, and their axons arborize in the immediate vicinity of the cell body. Most of these neurons are inhibitory, and they release either GABA or glycine. They synapse primarily on the cell body of the projection neurons but can also synapse on the dendrites of projection neurons as well as with each other. Two common types of pathways for these neurons (Figure 21-6A) include recurrent feedback pathways and feed-forward pathways. A special class of local circuit neurons in the spinal cord forms axoaxonic synapses on the terminals of sensory axons (Figure 21-6B). In some sensory pathways such as the retina and olfactory bulb, local circuit neurons may actually lack an axon and release neurotransmitter from dendritic synapses in a graded fashion in the absence of action potentials. 

Wakabayashi Y., Yagihashi T., Kezuka J., Muramatsu D., Usui M., and Iwasaki T. (2006). Glutamate levels in aqueous humor of patients with retinal artery occlusion. Retina 26 432 136. 

Ward M. M., Jobling A. I., Puthussery T., Foster L. E., and Fletcher E. L. (2004). Localization and expression of the glutamate transporter, excitatory amino acid transporter 4, within astrocytes of the rat retina. Cell Tissue Res. 315 305-310. 

Lucas and Newhouse (1957) firstly reported that subcutaneous injection of glutamate in neonatal rodents had toxic effect on the inner retinal layers. Later on, Sisk and Kuwabara (1985) demonstrated the susceptibility of adult retina to the intravitreal injection of glutamate, showing severe degeneration of the ganglion and inner nuclear layers (INLs). 

Glutamate is the major excitatory neurotransmitter in the retina where it is released by photoreceptors, bipolar, and ganglion cells (Yang, 2004). 

Several evidence underlie the crucial role of excessive glutamate release under ischemic conditions in the brain (Aarts el al., 2003 Camacho and Massieu, 2006 Dirnagl et al., 1999) and, concurrently, experimental data sustain a comparable role for glutamate under retinal ischemia (Adachi et al., 1998 Louzada-Junior et al., 1992). However, it should be stressed that the mechanisms underlying tolerance to ischemia may differ in brain and in the retina, the latter being more tolerant to ischemia than the former (Iijima et al., 2000 Osborne et al., 2004). 

Iijima, T., Iijima, C., Iwao, Y., and Sankawa, H. (2000). Difference in glutamate release between retina... 

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