Papers of the Week

Ca3.2, 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 Ca3.2 upregulation in the dorsal root ganglion. In mice, intraplantar TPEN also caused mechanical allodynia, which was abolished by T-channel inhibitors or Ca3.2 gene deletion. Together, spinal and peripheral zinc deficiency appears to enhance Ca3.2 activity in the spinal postsynaptic neurons and nociceptors, respectively, thereby promoting pain.