Store-operated Ca2+ entry in sensory neurons: functional role and the effect of painful nerve injury.

Painful nerve injury disrupts levels of cytoplasmic and stored Ca(2+) in sensory neurons. Since influx of Ca(2+) may occur through store-operated Ca(2+) entry (SOCE) as well as voltage- and ligand-activated pathways, we sought confirmation of SOCE in sensory neurons from adult rats and examined whether dysfunction of SOCE is a possible pathogenic mechanism. Dorsal root ganglion neurons displayed a fall in resting cytoplasmic Ca(2+) concentration when bath Ca(2+) was withdrawn, and a subsequent elevation of cytoplasmic Ca(2+) concentration (40 ± 5 nm) when Ca(2+) was reintroduced, which was amplified by store depletion with thapsigargin (1 μm), and was significantly reduced by blockers of SOCE, but was unaffected by antagonists of voltage-gated membrane Ca(2+) channels.

Axotomy depletes intracellular calcium stores in primary sensory neurons.

Background: The cellular mechanisms of neuropathic pain are inadequately understood. Previous investigations have revealed disrupted Ca signaling in primary sensory neurons after injury. The authors examined the effect of injury on intracellular Ca stores of the endoplasmic reticulum, which critically regulate the Ca signal and neuronal function.