Researchers have combined organ-on-a-chip engineering with the benefits of organoids to make improved models of the human retina.

Selective synapse formation in a retinal motion-sensitive circuit is orchestrated by starburst amacrine cells, which use homotypic interactions to initiate formation of a dendritic scaffold that recruits projections from circuit partners.

Synapse-specific genetic manipulations show that distinct GABAergic inputs are differentially recruited to encode motion direction in the retina in a stimulus-dependent manner.

Regulation of Pax6 expression through the α-enhancer fine-tunes amacrine cell subtype number, and consequently, the visual output of the retina.

Experimental and computational models reveal how parallel 'core' mechanisms shape direction selectivity at the dendrites of starburst amacrine cells and ganglion cells in the mouse retina.

Metabolic relationships between cells in the retina and retinal pigment epithelium are fundamental to retinal function, retinal disease and age-related vision loss and they may provide strategies for metabolism-based therapies.

Establishing retinal contrast transmission as a novel determinant of mammalian fitness, this research adds functional significance to a prominent exception of nuclear organization, previously described in nocturnal rod photoreceptor cells.

The Hippo pathway downstream effector YAP regulates S-phase progression to protect neural stem cells of the retina from experiencing genomic instability.

Existing artificial retinas produce distorted and imprecise activation of the visual system, but reverse engineering promises to refine the induced activation patterns.

Improved 3D and 4D imaging of neurovascular processes across scales reveals new insights into eye disease mouse models and shows retinal vessels are significantly distorted using standard flat-mount confocal imaging.