Increased expression of CaV3.2 T-type calcium channels in damaged DRG neurons contributes to neuropathic pain in rats with spared nerve injury.

Abstract

Ion channels are very important in the peripheral sensitization in neuropathic pain. Our present study aims to investigate the possible contribution of CaV3.2 T-type calcium channels in damaged dorsal root ganglion neurons in neuropathic pain. We established a neuropathic pain model of rats with spared nerve injury. In these model rats, it was easy to distinguish damaged dorsal root ganglion neurons (of tibial nerve and common peroneal nerve) from intact dorsal root ganglion neurons (of sural nerves). Our results showed that CaV3.2 protein expression increased in medium-sized neurons from the damaged dorsal root ganglions but not in the intact ones. With whole cell patch clamp recording technique, it was found that after-depolarizing amplitudes of the damaged medium-sized dorsal root ganglion neurons increased significantly at membrane potentials of -85 mV and -95 mV. These results indicate a functional up-regulation of CaV3.2 T-type calcium channels in the damaged medium-sized neurons after spared nerve injury. Behaviorally, blockade of CaV3.2 with antisense oligodeoxynucleotides could significantly reverse mechanical allodynia. These results suggest that CaV3.2 T-type calcium channels in damaged medium-sized dorsal root ganglion neurons might contribute to neuropathic pain after peripheral nerve injury.

• Authors: Xue-Jing Kang, Ye-Nan Chi, Wen Chen, Feng-Yu Liu, Shuang Cui, Fei-Fei Liao, Jie Cai, You Wan
• Journal: Molecular pain (Mol Pain) 2018 Jan-Dec Vol. 14 Pg. 1744806918765808 ISSN: 1744-8069 [Electronic] United States
• PMID: 29592785 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Cacna1h protein, rat
• Calcium Channels, T-Type
• RNA, Antisense

Topics

• Action Potentials
• Animals
• Calcium Channels, T-Type (metabolism)
• Cell Membrane (metabolism)
• Cell Size
• Ganglia, Spinal (metabolism, pathology)
• Gene Silencing
• Hyperalgesia (metabolism, pathology, physiopathology)
• Male
• Nerve Tissue (injuries, pathology)
• Neuralgia (metabolism, pathology)
• Neurons (metabolism)
• Nociception
• RNA, Antisense (metabolism)
• Rats, Sprague-Dawley
• Up-Regulation (genetics)