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Since<jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic>regulates sensory neuron excitability, altered CDI or CDF could contribute to pain generation after peripheral nerve injury. We explored this by manipulating [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>c<\/jats:sub>while recording<jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic>in rat sensory neurons. In uninjured neurons, elevating [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>c<\/jats:sub>with a conditioning prepulse (\u221215 mV, 2 s) inactivated<jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic>measured during subsequent test pulses (\u221215 mV, 5 ms). This inactivation was Ca<jats:sup>2+<\/jats:sup>-dependent (CDI), since it was decreased with elimination of Ca<jats:sup>2+<\/jats:sup>influx by depolarization to above the<jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic>reversal potential, with high intracellular Ca<jats:sup>2+<\/jats:sup>buffering (EGTA 10 m<jats:sc>m<\/jats:sc>or BAPTA 20 m<jats:sc>m<\/jats:sc>), and with substitution of Ba<jats:sup>2+<\/jats:sup>for extracellular Ca<jats:sup>2+<\/jats:sup>, revealing a residual voltage-dependent inactivation. At longer latencies after conditioning (&gt;6 s),<jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic>recovered beyond baseline. This facilitation also proved to be Ca<jats:sup>2+<\/jats:sup>-dependent (CDF) using the protocols limiting cytoplasmic Ca<jats:sup>2+<\/jats:sup>elevation. Ca<jats:sup>2+<\/jats:sup>\/calmodulin-dependent protein kinase II (CaMKII) blockers applied by bath (KN-93, myristoyl-AIP) or expressed selectively in the sensory neurons (AIP) reduced CDF, unlike their inactive analogues. Protein kinase C inhibition (chelerythrine) had no effect. Selective blockade of N-type Ca<jats:sup>2+<\/jats:sup>channels eliminated CDF, whereas L-type channel blockade had no effect. Following nerve injury, CDI was unaffected, but CDF was eliminated in axotomized neurons. Excitability of sensory neurons in intact ganglia from control animals was diminished after a similar conditioning pulse, but this regulation was eliminated by injury. These findings indicate that<jats:italic>I<jats:sub>Ca<\/jats:sub><\/jats:italic>in sensory neurons is subject to both CDI and CDF, and that hyperexcitability following injury-induced loss of CDF may result from diminished CaMKII activity.<\/jats:p>","DOI":"10.1523\/jneurosci.0983-12.2012","type":"journal-article","created":{"date-parts":[[2012,8,22]],"date-time":"2012-08-22T16:34:30Z","timestamp":1345653270000},"page":"11737-11749","source":"Crossref","is-referenced-by-count":29,"title":["Ca<sup>2+<\/sup>-Dependent Regulation of Ca<sup>2+<\/sup>Currents in Rat Primary Afferent Neurons: Role of CaMKII and the Effect of Injury"],"prefix":"10.1523","volume":"32","author":[{"given":"Qingbo","family":"Tang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madhavi Latha Yadav","family":"Bangaru","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra","family":"Kostic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Pan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hsiang-En","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew S.","family":"Koopmeiners","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongwei","family":"Yu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory J.","family":"Fischer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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