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Differences in kinetics of retinal output signals originate at least in part from differences in synaptic output from distinct bipolar cell types.

The T-shaped fold of an abundant surface protein ties streptococci to collagens, an interaction that enhances biofilm such as often found in invasive infections.

Afadin-deficient mice, whose outer-retinal lamination and photoreceptor synapses are severely disrupted, nonetheless partially retain retinal neural circuits and visual function.

Optogenetic climbing fiber activation regulates experience-dependent plasticity in the primary somatosensory cortex of mice, suggesting a role of the olivo-cerebellum in instructive signaling across brain regions.