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J. Johnson, V. R. Wu, R. H. Edwards, D. R. Copenhagen; Vesicular Glutamate Release From Photoreceptors is Required for Maintenance, but Not Formation of Synapses in the Outer Retina. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5946.
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Previous studies have found that mutations that regulate intracellular calcium or synaptic ribbon structure lead to morphological deterioration of pre and post-synaptic structures in the outer plexiform layer (OPL). These mutations effect exocytosis of synaptic vesicles. It is not clear if vesicular release of glutamate itself is sufficient for formation and maintenance of these synapses or is due instead to the release of another trophic factor. We addressed this question by examining pre and post synaptic structures in a mouse line (VGLUT1 null) in which exocytosis occurs in the absence of vesicular glutamate release.
We used immunohistochemistry and electron microscopy to examine pre and post-synaptic structure in the OPL.
In young VGLUT1 null mice, just after eye-opening, photoreceptor synaptic markers and horizontal and bipolar cell labeling appeared normal, indicating normal structural formation of these synapses. However, there is no detectable functional synaptic transmission from photoreceptors to second order cells. In adult mice there was significant disruption of the OPL. The OPL was thinner and numerous ectopic extensions of rod bipolar and horizontal cells were observed. Photoreceptor presynaptic markers in the ONL colocalized with horizontal and bipolar extensions, suggesting that these represent ectopically formed synapses. Surprisingly, horizontal and bipolar ectopic neurite extensions were often found to colocalize. In addition, the synaptic morphology of rod photoreceptor terminals was compromised.
Vesicular glutamate release is not necessary for the normal early formation of pre and post-synaptic structures in the outer retina, but is essential for maintenance. The VGLUT1 null mouse, which has presumed normal exocytosis, but lacks vesicular release of glutamate, is a valuable model for examining the role of glutamate in the formation and preservation of synapses in the outer retina.
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