The Role of Protons in the Activation of Primary Sensory Neurons

Abstract

Primary sensory neurons with cell bodies localized to trigeminal, vagal and dorsal root ganglia (DRG) consist of different subpopulations of pseudounipolar neurons distinguished according to their phenotype, velocity of impulse conduction, neurotransmitter content and type of stimulus that they recognize. Among these diverse subpopulations, a group of neurons exists that are uniquely stimulated by capsaicin and that express and release from their central and peripheral terminals neuropeptide transmitters. Capsaicin, better known as the hot principle contained in the plants of the genus Capsicum, is a vanilloid derivative that exerts multiple and specific actions on primary sensory neurons[1]. These actions somehow resemble those exerted by guanethidine on sympathetic neurons. At low concentrations, capsaicin excites neurons of in vitro preparations by promoting cation influx (Na1 and Ca1) into the nerve terminal. This event initiates a propagated action potential that orthodromically invades the neurons, thus conveying the sensory information to the lamina I and II of the dorsal spinal cord and medulla oblongata. The consequence of this effect (often appreciated when small quantities of capsaicin are added to food) is a hot and burning sensation that usually fades in a few minutes without any appreciable tissue damage.