Abstract
Vision in dim light depends on synapses between rods and rod bipolar cells (RBCs). Here, we find that these synapses exist in multiple configurations, in which single release sites of rods are apposed by one to three postsynaptic densities (PSDs). Single RBCs often form multiple PSDs with one rod; and neighboring RBCs share ~13% of their inputs. Rod-RBC synapses develop while ~7% of RBCs undergo programmed cell death (PCD). Although PCD is common throughout the nervous system, its influences on circuit development and function are not well understood. We generate mice in which ~53 and ~93% of RBCs, respectively, are removed during development. In these mice, dendrites of the remaining RBCs expand in graded fashion independent of light-evoked input. As RBC dendrites expand, they form fewer multi-PSD contacts with rods. Electrophysiological recordings indicate that this homeostatic co-regulation of neurite and synapse development preserves retinal function in dim light.
Highlights
Vision in dim light depends on synapses between rods and rod bipolar cells (RBCs)
We observed a range of RBC postsynaptic densities (PSDs) containing the probable G-protein coupled receptor 179 (Gpr179)[38,39,40] in individual rod spherules (Fig. 1a, b)
The distribution of RBC postsynaptic specializations per rod was similar when we stained for the metabotropic glutamate receptor mGluR63, 41 instead of Gpr[179], and when super-resolution rather than conventional confocal microscopy was used
Summary
Vision in dim light depends on synapses between rods and rod bipolar cells (RBCs). Here, we find that these synapses exist in multiple configurations, in which single release sites of rods are apposed by one to three postsynaptic densities (PSDs). We generate mice in which ~53 and ~93% of RBCs, respectively, are removed during development In these mice, dendrites of the remaining RBCs expand in graded fashion independent of light-evoked input. Throughout the developing nervous system, many neurons undergo programmed cell death (PCD), adjusting the complement and density of neuronal populations in emerging circuits[25, 26]. Cell density-dependent plasticity has been shown to regulate axon and dendrite growth of some retinal neurons[29, 30] but not others[31, 32]. To analyze the influence of cell density-dependent plasticity on RBC development and retinal circuit function, we generated mice in which ~53 and ~93% of RBCs, respectively, are removed by transgenic expression of diphtheria toxin concurrent with naturally occurring PCD26. This coordinated plasticity of neurites and synapses occurs independent of light-evoked input from rods and preserves retinal output in dim light
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