Cadherin-dependent cell adhesion controls the contralateral migration and clustering of ocular motor subpopulations and is required for the development of functional eye movements driven by those neurons.

Spiking networks compensate the loss of neurons instantaneously, when restoration of excitatory/inhibitory balance becomes equivalent to restoration of functionality.

Involuntary eye movements that keep images positioned over the center of the retina are synchronized with blinks to minimize disruption to vision.

High-resolution foveal imaging and micro-psychophysics reveal that the human oculomotor system finely adjusts drift motion of the eye in an acuity task to enhance retinal sampling, achieving sub-cell resolution.

The capacity for new cerebellum-dependent learning is influenced by the recent history of neural activity in a mouse model of Fragile X syndrome, suggesting a role for metaplasticity.

An accurate, robust, and lightweight technique for measuring eye movements in mice was developed using magnetic sensing, yielding the first high resolution recordings of eye movements in freely moving mice.

Non-invasive disinhibition of the oculomotor system shows that ongoing preparatory activity in the superior colliculus has movement-generating potential and need not rise to threshold in order to produce a saccade.

A comprehensive modeling approach reconciles experimental observations with classic plasticity mechanisms in the cerebellar cortex, demonstrating how learning-related changes in neural activity can appear to contradict the sign of the underlying plasticity when feedback is present.

Fixational eye movements transform the spatial scene into temporal modulations on the retina, which, together with the known sensitivities of retinal neurons, provide a comprehensive account of human spatial sensitivity.

Recordings of ear muscles in humans show that ears attempt to pivot in the direction that requires attention.