The present study reports that intracisternal administration of capsaicin induces the selective degeneration of chemosensitive primary sensory afferents and results in a practically complete abolition of chemical pain sensitivity in the adult rat. This treatment, however, failed to affect neurogenic inflammation in the corresponding skin areas. Accordingly, intracisternal capsaicin induces merely the degeneration of the centrally directed axons of chemosensitive primary sensory neurons (CPSNs). To indicate their particular dual function, CPSNs are proposed to be termed secreto-sensory nociceptive neurones. It is suggested that these neurons, through the release of neurogenic factor(s) at their peripheral end, may effectively modulate the afferent input related to pain sensation at the level of sensory receptors.