Effect of electrical field stimulation on dorsal root ganglion neuronal function.

Objectives: Neural stimulation may provide analgesia for a variety of painful conditions. Activation of primary sensory neurons, which underlies pain relief by spinal cord stimulation, also may be achieved by stimulation at the level of the dorsal root ganglion (DRG). The DRG also is a site of pain pathogenesis, particularly in neuropathic pain.

Ca²⁺-dependent regulation of Ca²⁺ currents in rat primary afferent neurons: role of CaMKII and the effect of injury.

Currents through voltage-gated Ca²⁺ channels (I(Ca)) may be regulated by cytoplasmic Ca²⁺ levels ([Ca²⁺](c)), producing Ca²⁺-dependent inactivation (CDI) or facilitation (CDF). Since I(Ca) regulates sensory neuron excitability, altered CDI or CDF could contribute to pain generation after peripheral nerve injury. We explored this by manipulating [Ca²⁺](c) while recording I(Ca) in rat sensory neurons.

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 Dorsal root ganglion neurons displayed a fall in resting cytoplasmic Ca(2+) concentration when bath Ca(2+) was withdrawn, and a subsequent elevation of cytoplasmic Ca(2+) concentration (40 ± 5 nm) when Ca(2+) was reintroduced, which was amplified by store depletion with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.

Calcium signaling in intact dorsal root ganglia: new observations and the effect of injury.

Background: Ca is the dominant second messenger in primary sensory neurons. In addition, disrupted Ca signaling is a prominent feature in pain models involving peripheral nerve injury. Standard cytoplasmic Ca recording techniques use high K or field stimulation and dissociated neurons.