Abstract

A specialized subpopulation of unmyelinated chemonociceptors and dedicated spinal neurons which are responsible for the itch sensation have been identified recently. Under physiological conditions, painful stimuli such as activation of conventional mechano-heat-sensitive ('polymodal') nociceptors (scratching) inhibit the itch sensation via central mechanisms. Conversely, centrally acting pain-inhibiting opioids enhance itch by disinhibition. These mechanisms might well explain the itch in diseases characterized by histamine release like urticaria, and might provide evidence for the role of endogenous opioids as central itch promotors in cholestasis or nephropathy. After the discovery of itch-specific neurons has dramatically improved our understanding of itch mechanisms under experimental conditions, the present task is to correlate these new findings to the clinical situation of itch patients.