Presynaptic development is controlled by the core active zone proteins CAST/ELKS.

Key Points: CAST/ELKS are positive regulators of presynaptic growth and are suppressors of active zone expansion at the developing mouse calyx of Held. CAST/ELKS regulate all three Ca 2 subtype channel levels in the presynaptic terminal and not just Ca 2.1.

Ca2.1 α Subunit Expression Regulates Presynaptic Ca2.1 Abundance and Synaptic Strength at a Central Synapse.

The abundance of presynaptic Ca2 voltage-gated Ca channels (Ca2) at mammalian active zones (AZs) regulates the efficacy of synaptic transmission. It is proposed that presynaptic Ca2 levels are saturated in AZs due to a finite number of slots that set Ca2 subtype abundance and that Ca2.1 cannot compete for Ca2.

CAST/ELKS Proteins Control Voltage-Gated Ca Channel Density and Synaptic Release Probability at a Mammalian Central Synapse.

In the presynaptic terminal, the magnitude and location of Ca entry through voltage-gated Ca channels (VGCCs) regulate the efficacy of neurotransmitter release. However, how presynaptic active zone proteins control mammalian VGCC levels and organization is unclear. To address this, we deleted the CAST/ELKS protein family at the calyx of Held, a Ca2.

A novel region in the Ca2.1 α subunit C-terminus regulates fast synaptic vesicle fusion and vesicle docking at the mammalian presynaptic active zone.

In central nervous system (CNS) synapses, action potential-evoked neurotransmitter release is principally mediated by Ca2.1 calcium channels (Ca2.1) and is highly dependent on the physical distance between Ca2.