CACNA1B is a voltage-gated calcium channel alpha subunit. It is expressed almost exclusively in neurons typically located at high densities in presynaptic terminals. Opening of these channels enables the rapid influx of the extracellular Ca2+, triggering exocytotic vesicle fusion with terminal membranes and subsequent neurotransmitter release. Evidence suggests that Cav2.2 channels have a fundamental role in instigating increased excitability and neurotransmitter release in various pain syndromes. The link between CACNA1B and pain neurotransmission in humans has been further vindicated by the effectiveness of PrialtR (ziconotide), a synthetic version of omega-conotoxin MVIIA, in treating severe chronic pain.