Following tissue injury, both peripheral and central sensory neurons can become hyperexcitable, or "sensitized." Sensitization can lead to long-term pathological changes in pain sensation. Because many chronic pain conditions are refractory to most currently available treatments, there is great interest in identifying molecular targets that contribute to the sensitization of sensory neurons. Among these, several classes of ion channels have emerged as potential targets. Recent in vitro and in vivo studies have demonstrated a role for T-type Ca2+ channels in sensory pathways and have suggested that these channels may contribute to pain processing and sensitization. Therefore, T-type channels may represent an opportunity for the development of novel pain therapeutics and may help to address an unmet medical need.