{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T03:10:29Z","timestamp":1793329829825,"version":"4.5.0"},"reference-count":64,"publisher":"Society for Neuroscience","issue":"3","license":[{"start":{"date-parts":[[2010,7,20]],"date-time":"2010-07-20T00:00:00Z","timestamp":1279584000000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2010,1,20]]},"abstract":"<jats:p>\n                    The maintenance of chronic pain states requires the regulation of gene expression, which relies on an influx of calcium. Calcium influx through neuronal L-type voltage-gated calcium channels (LTCs) plays a pivotal role in excitation\u2013transcription coupling, but the involvement of LTCs in chronic pain remains unclear. We used a peptide nucleic acid (transportan 10-PNA conjugates)-based antisense strategy to investigate the role of the LTC subtypes Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2 and Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.3 in long-term pain sensitization in a rat model of neuropathy (spinal nerve ligation). Our results demonstrate that specific knockdown of Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2 in the spinal dorsal horn reversed the neuropathy-associated mechanical hypersensitivity and the hyperexcitability and increased responsiveness of dorsal horn neurons. Intrathecal application of anti-Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2 siRNAs confirmed the preceding results. We also demonstrated an upregulation of Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2 mRNA and protein in neuropathic animals concomitant to specific Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2-dependent phosphorylation of the cAMP response element (CRE)-binding protein (CREB) transcription factor. Moreover, spinal nerve ligation animals showed enhanced transcription of the CREB\/CRE-dependent gene COX-2 (cyclooxygenase 2), which also depends strictly on Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2 activation. We propose that L-type calcium channels in the spinal dorsal horn play an important role in pain processing, and that the maintenance of chronic neuropathic pain depends specifically on channels comprising Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2.\n                  <\/jats:p>","DOI":"10.1523\/jneurosci.3145-09.2010","type":"journal-article","created":{"date-parts":[[2010,1,20]],"date-time":"2010-01-20T15:23:27Z","timestamp":1264001007000},"page":"1073-1085","source":"Crossref","is-referenced-by-count":104,"title":["Knockdown of L Calcium Channel Subtypes: Differential Effects in Neuropathic 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