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.

Subacute ibuprofen treatment rescues the synaptic and cognitive deficits in advanced-aged mice.

Aging is accompanied by increased neuroinflammation, synaptic dysfunction, and cognitive deficits both in rodents and humans, yet the onset and progression of these deficits throughout the life span remain unknown. These aging-related deficits affect the quality of life and present challenges to our aging society. Here, we defined age-dependent and progressive impairments of synaptic and cognitive functions and showed that reducing astrocyte-related neuroinflammation through anti-inflammatory drug treatment in aged mice reverses these events.