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Structure modeling, site-directed mutagenesis, and current recordings revealed the mechanism by which stabilization of voltage sensors in the resting and activated states determines the gating properties of the Ca_V1.1 calcium channel.

Modulation of the energy barrier for membrane fusion is a common mechanism by which sensors in the synapse produce supralinear calcium dependence of vesicle release and short-term synaptic potentiation.

The neuronal calcium sensor Neurocalcin regulates sleep and arousal thresholds during the night in Drosophila.

Nanodomain clustering of cAMP effectors represents a novel mechanism of cAMP compartmentation within an oscillatory signaling circuit.

Slow presynaptic depression in olfactory receptor neurons rescales combinatorial odor representations in postsynaptic neurons and mediates the encoding of stimulus mean and variance.

The analytic theory establishes the general principles of synaptic transmission, enables extraction of microscopic parameters of synaptic fusion machinery from experiments, and links molecular constituents to synaptic function.

Axon degeneration occurs via an ordered sequence of events downstream of SARM1 that proceeds from ATP loss, to defects in mitochondrial movement and depolarization, followed by calcium influx, phosphatidylserine externalization, loss of membrane permeability, and ending with catastrophic axonal self-destruction.

Purinergic keratinocyte-to-sensory neuron signaling is a ubiquitous amplification mechanism that is required for normal mechanical, cold, and heat sensation in vivo.

Simultaneous voltage and calcium two-photon imaging of Purkinje neuron dendrites in awake mice reveals multiple interplaying mechanisms underlying sensory-evoked dendritic coincidence detection of parallel fiber and climbing fiber input.

Ca²⁺ channels and release sensors at a fast central synapse are tightly coupled, which minimizes the effect of extracellular Ca²⁺ concentration on the timing of transmitter release.