2007
DOI: 10.1002/cne.21609
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Early afferent signaling in the outer plexiform layer regulates development of horizontal cell morphology

Abstract: The pedicles of cone photoreceptors, labeled with an antibody to mouse cone arrestin (blue), stratify in the outer plexiform layer, where they form synapses with the dendrites of horizontal and bipolar cells. Those synaptic sites are evidenced by the co‐localization of the synaptic ribbon protein, piccolo (red), with the cone arrestin labeling. The remaining red profiles in the outer plexiform layer indicate the sites of the rod spherules. An antibody to cytochrome oxidase (green) labels the mitochondrion‐rich… Show more

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Cited by 4 publications
(4 citation statements)
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“…In transgenic mice lacking all cones, their dendritic fields are largely barren of higher-order dendritic branches and clustered terminal endings, while in “conefull” mice (in which all of the rods are re-specified to become cones), their fields have hypertrophied, filling the entire field-area with branches that occupy the full depth of the outer plexiform layer (Raven et al, 2007; Reese et al, 2005). Dark-rearing does not reproduce the horizontal cell phenotype observed in the coneless mouse, but the Cacna1f -mutant mouse does, disrupting all synaptic transmission in the outer plexiform layer due to defective calcium channel assembly in the photoreceptor terminals (Raven et al, 2008). This developmental plasticity of the horizontal cell is all the more striking in the absence of similar changes in the other primary target of the cone pedicles in the outer plexiform layer, the cone bipolar cells (Keeley & Reese, 2010b).…”
Section: Development Of the Retinamentioning
confidence: 99%
“…In transgenic mice lacking all cones, their dendritic fields are largely barren of higher-order dendritic branches and clustered terminal endings, while in “conefull” mice (in which all of the rods are re-specified to become cones), their fields have hypertrophied, filling the entire field-area with branches that occupy the full depth of the outer plexiform layer (Raven et al, 2007; Reese et al, 2005). Dark-rearing does not reproduce the horizontal cell phenotype observed in the coneless mouse, but the Cacna1f -mutant mouse does, disrupting all synaptic transmission in the outer plexiform layer due to defective calcium channel assembly in the photoreceptor terminals (Raven et al, 2008). This developmental plasticity of the horizontal cell is all the more striking in the absence of similar changes in the other primary target of the cone pedicles in the outer plexiform layer, the cone bipolar cells (Keeley & Reese, 2010b).…”
Section: Development Of the Retinamentioning
confidence: 99%
“…In the developing central nervous system (CNS), electrical activity and spontaneous release of neurotransmitters influence neural proliferation, migration and neuronal differentiation, including neurotransmitter specification, neuronal morphology, and axon guidance 1–6 . For example, endogenous GABA and glutamate influence the speed of migration of neurons in a number of regions of the developing brain, 7–9 control neuroblast number in proliferative zones, 10 and regulate the neurotransmitter phenotype of neurons in the developing spinal cord 11 .…”
mentioning
confidence: 99%
“…Similarly, we found GABA was lost by P7, matching cone synaptogenesis in the mouse retina which occurs at P6 (Blanks et al, 1974). Raven et al (2008) found horizontal cells express a calcium channel during development essential for normal cone pedicle formation, suggesting horizontal cells play a pivotal role in OPL development. However, few morphological defects were observed on the cone pedicles of mice where the GABA synthesizing enzyme, GAD 67 was knocked out of horizontal cells (Schubert et al, 2010).…”
Section: Discussionmentioning
confidence: 96%