Mouse retina maps link energy supply with the organisation of signal release
A peer-reviewed mouse study mapped the arrangement of energy-producing mitochondria, synaptic ribbons and signalling vesicles in light-sensitive retinal cells. Rods and cones had different structures. Changes to a mitochondrial anchoring protein accompanied stronger electrical responses, although the protein may also influence release through other routes. No treatment for human vision was tested.
Science··Midday
Rods and cones organise their signal terminals differently
A peer-reviewed mouse study mapped how mitochondria, synaptic ribbons and signalling vesicles fit together at the ends of light-sensitive retinal cells. Mitochondria supply energy, while ribbons help organise the vesicles that release chemical signals to neighbouring cells. Three-dimensional electron microscopy showed different architectures in rods and cones, the retina's two broad classes of light detectors. A typical rod terminal had a single ribbon beside one large mitochondrion. Cone terminals contained multiple mitochondria and more distributed ribbons.[1]
An anchoring-protein change accompanies stronger signals
Mice lacking syntaphilin, a protein that anchors mitochondria, had more mitochondria at conventional rod terminals and larger vesicle pools in some comparisons. Electrical measurements of the retina showed larger responses under different light conditions. Particular bipolar cells, which receive signals from photoreceptors, experienced more frequent spontaneous excitatory currents without a corresponding increase in their amplitude. Syntaphilin can also affect release proteins through other routes, limiting attribution of the electrical change solely to mitochondrial abundance.[1]
A degeneration model shows the structure coming apart
The team also examined a model of retinal degeneration. Mitochondria lost their normal shape, while ribbons partly detached and vesicles spread out. That model begins with a Pde6b gene mutation, so the disassembly does not establish mitochondria as the initiating cause of degeneration. Healthy electron-microscopy reconstructions used three mice; one cone subtype was represented by only two terminals. The structural and electrical observations concern mouse cells, with no human vision treatment tested.[1]
