Some of the earliest detailed descriptions of biophysical properties of low voltage-activated (LVA) or transient (T) type Ca2+ channels were done using in vitro preparation of primary sensory or dorsal root ganglion (DRG) neurons that are known for their functional role in processing pain signals. However, in spite of these early discoveries, T-type channels were not implicated in sensory transmission in general and pain processing (nociception) in particular until recently. New evidence obtained using an array of techniques such as electrophysiological recordings, pharmacological behavioral experiments as well as molecular techniques strongly supports the role of peripheral T-type Ca2+ channels in boosting nociceptive transmission in a variety of experimental pain models. Therefore, these channels in peripheral sensory neurons may be the important, although previously unappreciated, targets for novel pain therapies. In this article, we review past, present and future findings aimed at illuminating the role of peripheral T-type Ca2+ channels in nociception and the value of these channels as cellular targets for potential drug developments.