| 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 Ih 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. |