| abstract |
Markedly enhanced activity of pacemaker (hyperpolarization-activated, cation-nonselective, HCN) ion channels governs spontaneous firing in sensory cells of allodynic rats. An HCN ion channel specific blocker, ZD7288, dose-dependently and completely suppresses allodynia. Nerve injury increases the population of large DRG neurons expressing a high density of I h and modulates HCN mRNA expression. New methods of treating pain by targeting HCN pacemaker channels are developed. In addition, new methods for identifying compositions useful for treating pain are disclosed. |