Abstract
Purpose: Recent studies have shown that compromised photoreceptor synaptic transmission results in morphological deterioration of pre and post-synaptic structures in the retinal outer plexiform layer (OPL). Interestingly, similar synaptic disruption is seen in human aged and diseased retina. It is not clear if vesicular release of glutamate itself is necessary for maintenance of these synapses. We addressed this question by examining pre and post synaptic structures in a mouse line that lacks vesicular glutamate 1 (VGLUT1). Loss of VGLUT1 abolishes synaptic transmission from photoreceptors. Methods: We used immunohistochemistry and electron microscopy to examine pre and post-synaptic structure in the OPL. Results: In young VGLUT1 null mice, just after eye-opening, photoreceptor synaptic markers and horizontal and bipolar cell labeling appeared normal. In adult VGLUT1 null mice, starting at one month of age, there was significant disruption of the OPL. Conclusions: Vesicular glutamate release is not necessary for the early formation of pre and post-synaptic structures in the OPL, but is essential for maintenance. The VGLUT1 null mouse is a valuable model for examining and testing therapeutic treatments to diminish synaptic remodeling of the OPL, which occurs in both aged and diseased retina.