Capsaicin, the main pungent ingredient in 'hot' red peppers, selectively stimulate pain transmitting primary afferent nerve fibers by activating specific vanilloid (VR1) receptors. Capsaicin administration to the neonatal rat results in lifelong insensitivity to the noxious stimuli accompanied by destruction of the unmyelinated and lightly myelinated fibers as well as small B type dorsal root ganglion neurons, but capsaicin effects on adult animals were reversible. Since the discovery of the action of capsaicin, this agent attract many active investigators because of their selective degenerative action on pain transmitting unmyelinated nerve fibers. Effects of capsaicin on the morphology of nervous system were reviewed. In summary, capsaicin decrease the number of substance P- and CGRP-immunoreactive neuronal cell bodies in dorsal root ganglion and decrease the densities and areas of substance P- and CGRP immunoreactive terminals in the dorsal horn. Capsaicin also decrease the number of c-fos immunoreactive dorsal horn neurons activated by painful stimuli. Recently, capsaicin and capsaicinoids are being studied as effective pharmacological agents for a number of sensory nerve fiber disorders, including pain associated with rheumatoid arthritis, osteoarthritis, diabetic neuropathy, and bladder disorders. Capsaicin appears to be a promising prototype for obtaining selective analgesia in diverse pain syndromes.