Proteolytic maturation of auxiliary α2δ subunits of voltage-gated calcium channels increases neuronal communication by controlling the synaptic release of neurotransmitter.

Proteomic and genetic analysis discovers a new cytoskeletal mechanism of presynaptic short-term plasticity common across neuronal cell types.

Voltage-gated calcium channel delivery to synaptic active zones (AZs) occurs broadly across the population, correlates with AZ size, and is regulated by α2δ, while channel recycling is promoted by new delivery to generate an upper limit on AZ accumulation.

The anchoring properties of Ca_V β2 subunits to the plasma membrane determine the biophysical states of Ca_V2.2 channels by regulating PIP₂ coupling to the nonspecific phospholipid-binding site in the I–II loop.

Maladaptive changes of pro-nociceptive neurons in the central nucleus of the amygdala drive the chronification of muscle pain and comorbid affective behaviors.

In vivo analysis of endogenously tagged Ca²⁺ channel subunits reveals unexpected differences in subunit composition and synapse-specific relationships between channel abundance and synaptic strength.