Neonatal capsaicin treatment has been shown to cause selective degeneration of chemosensitive primary sensory neurons involved in the mediation of chemogenic pain and in neurogenic inflammatory responses. In the present study the neurotoxic effect of capsaicin congeners was investigated in the newborn rat. Some quantitative data on the selective neurotoxic action of capsaicin are also reported. Electron microscopy indicates that some pungent congeners of capsaicin also induce the selective degeneration of type 'B' sensory ganglion cells. At high doses the distribution pattern of axon terminal degeneration within the spinal cord and brain stem was equivalent to that observed after neonatal capsaicin treatment. The neurotoxic potency of capsaicin congeners, unlike desensitizing activity, is closely related to the sensory irritant property of these compounds. It is concluded that primary sensory neurons degenerating after the administration of these capsaicin congeners may correspond to substance P-containing chemosensitive primary sensory neurons involved in the transmission of nociceptive impulses.