| First Author | Tomita S | Year | 2023 |
| Journal | J Pharmacol Sci | Volume | 152 |
| Issue | 2 | Pages | 86-89 |
| PubMed ID | 37169483 | Mgi Jnum | J:359627 |
| Mgi Id | MGI:7788530 | Doi | 10.1016/j.jphs.2023.03.007 |
| Citation | Tomita S, et al. (2023) Ca(v)3.2-dependent hyperalgesia/allodynia following intrathecal and intraplantar zinc chelator administration in rodents. J Pharmacol Sci 152(2):86-89 |
| abstractText | Ca(v)3.2, a T-type calcium channel (T-channel) family member, is expressed in the nociceptors and spinal cord, and its activity is largely suppressed by zinc under physiological conditions. In rats, intrathecal and intraplantar administration of a zinc chelator, TPEN, caused T-channel-dependent mechanical hyperalgesia, and the intraplantar, but not intrathecal, TPEN induced Ca(v)3.2 upregulation in the dorsal root ganglion. In mice, intraplantar TPEN also caused mechanical allodynia, which was abolished by T-channel inhibitors or Ca(v)3.2 gene deletion. Together, spinal and peripheral zinc deficiency appears to enhance Ca(v)3.2 activity in the spinal postsynaptic neurons and nociceptors, respectively, thereby promoting pain. |
