Axotomy prevents capsaicin-induced sensory ganglion cell degeneration

Abstract

A particular group of mammalian primary afferent neurons involved in nociception is characterized by its specific sensitivity to capsaicin, the pungent principle of red pepper. A striking manifestation of neuronal capsaicin sensitivity is the degeneration of a morphologically well characterized population of sensory ganglion cells following a systemic injection of this compound. The present study demonstrated that prior transection of the peripheral axons of these neurons protects them from the neurotoxic action of systemically administered capsaicin. It is suggested that this phenomenon is related to an impairment of axon transport mechanisms. It is concluded that maintenance of capsaicin sensitivity is critically dependent on the integrity of the peripheral branch of the primary sensory neuron and peripherally derived trophic factor(s) may profoundly influence the functional traits of sensory ganglion cells.