By regulating protein translation within the neuron, insulin signaling can control neuronal activity by altering the release of neurotransmitter molecules.

Photobleaching and recovery of a fluorescent glutamate sensor enable demonstration of the distinct spatial architectures of spontaneous versus evoked forms of glutamatergic neurotransmission within single synapses.

During development, lateral processes of retinal Müller glia are highly motile, and this motility persists when retinal waves and calcium transients are blocked, suggesting that Müller glial morphology is established independent of neuronal activity.

GABAergic postsynaptic responses mediated by spontaneous and evoked neurotransmitter release are partially segregated, suggesting they may serve distinct roles in neuronal signaling.

Targeting a genetically-encoded glutamate sensor to postsynaptic sites demonstrates the feasibility of simultaneous optical quantal analysis of many inputs to a neuron in wide-field fluorescence microscopy.

In vivo imaging reveals that the synaptic vesicle cycle is a significant contributor to oxidative stress in sensory hair cells, rendering them susceptible to insults.

Targeted genetic silencing and reporter labeling reveal that Purkinje cell activity organizes cerebellar basket cells into zonal modules based on the sizes of their projections.

A combination of electrophysiological, electrochemical, and anatomical experiments sheds new light on how the complex neurotransmitter repertoire of dopaminergic neurons in the brain is regulated by proteins of the neurexin family.

In a population of mammalian central synapses, spontaneous and evoked neurotransmitter release processes are independently distributed; yet, postsynaptic receptors within a single synapse preferentially receive neurotransmitter from only one mode of release.

Neurotransmission pathways from primary to secondary neurons encode odor and underlie age-related sensory behavioral declines.