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Electrical synapses in rod and cone pathways of the mouse retina

Subject Area Cognitive, Systems and Behavioural Neurobiology
Molecular Biology and Physiology of Neurons and Glial Cells
Term from 2015 to 2019
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 270305961
 
Final Report Year 2019

Final Report Abstract

The mammalian retina is able to encode visual information over ~10 log units of light intensities. It therefore has evolved two types of photoreceptors: rods for vision under dim light and cones for vision under bright light and color vision. Electrical synapses (gap junctions) built from connexin proteins play an essential role in the most sensitive rod pathway, the primary rod pathway, and in cone pathways. In the primary rod pathway, dim light signals are mediated from rods to rod bipolar cells, which in turn contact AII amacrine cells. AII cells form homocellular gap junctions among each other, thereby optimizing signal-to-noise ratio when photons are scarce. AII cells send the rod signal via glycinergic synapses to OFF cone bipolar cells and via heterocellular gap junctions to ON cone bipolar cells. Additionally, another small-field amacrine cell makes gap junctions with ON cone bipolar cells, the A8 cell. In this project, we aimed to determine the molecular basis for the differences in structure, assembly, and light-dependent modulation of homo- and heterocellular AII gap junctions and A8 gap junctions. To achieve our goals, we used co-immunoprecipitation, tracer coupling experiments, and (super-resolution) microscopy-based quantitative analyses of connexin localization. We found that AII amacrine cells express not only connexin36 but also connexin30.2 and showed that the two connexins are able to form heteromeric gap junctions. However, the role of connexin30.2 in AII cells remains enigmatic because the deletion of connexin30.2 did not impair the rod pathway in any way. As AII gap junctions were shown to be regulated by CaMKII in an activity-dependent manner, we determined the CaMKII isoform involved in this process. We found that expression of CaMKII isoforms is cell-type specific in the retina, with CaMKII-δ being the dominant isoform in AII cells and CaMKII-β in A8 cells. A8 and AII cells did not only differ in the CaMKII isoform they express but also in coupling partners, gap junction number, and gap junction modulation. In summary, our study helped to understand how electrically coupled retinal neurons are able to establish electrical synapses with different synaptic partners and how these synapses can be differentially modulated. It also suggested that gap junctions may also serve signal facilitation or amplification in some retinal neurons.

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