The Role of Protons in the Activation of Primary Sensory Neurons
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. 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.
KeywordsDorsal Root Ganglion Primary Sensory Neuron Neurogenic Inflammation Plasma Extravasation Dural Venous Sinus
Unable to display preview. Download preview PDF.
- 3.Geppetti P (1996) Capsaicin as a drug. In: Geppetti P, Holzer P (eds) Neurogenic inflammation. CRC, Boca Raton, 289–298Google Scholar
- 10.Maggi C, Giuliani S (1991) The neurotransmitter role of calcitonin gene-related peptide in the rat and guinea-pig ureter: effect of calcitonin gene-related peptide antagonist and species-related differences in the action of omega conotoxin on calcitonin gene-related peptide release from primary afferents. Neuroscience 43:261–268PubMedCrossRefGoogle Scholar
- 12.Hall JM, Brain SD (1996) Pharmacology of calcitonin gene-related peptide. In: Geppetti P, Holzer P (eds) Neurogenic inflammation. CRC, Boca Raton, 101–114Google Scholar
- 16.Advenier C, Daoui S, Cui YY, Lagente V, Emonds-Alt X (1996) Inhibition by the tachykinin NK3 receptor antagonist, SR 142801, of substance P-induced microvascular leakage hypersensitivity and airway hyperresponsiveness in guinea-pigs. Am J Respir Crit Care Med 153:A163Google Scholar
- 17.Szolcsanyi J (1984) Capsaicin-sensitive chemoceptive neural system with dual sensory-efferent function. In: Chahl LA, Szolcsanyi J, Lembeck F (ed) Antidromic vasodilatation and neurogenic inflammation. Akademiai Kiado, Budapest, 27–56Google Scholar
- 35.Del Bianco E, Santicioli P, Tramontana M, Maggi CA, Cecconi R, Geppetti P (1991) Different pathways by which extracellular Ca2+ promotes calcitonin gene-related peptide release from central terminals of capsaicin-sensitive afferents of guineapigs: effect of capsaicin high K+ and low pH media. Brain Res 566:46–53PubMedCrossRefGoogle Scholar
- 36.Bevan S, Yeats J (1991) Protons activate a cation conductance in a sub-population of rat dorsal root ganglion neurones. J Physiol (Lond) 433:145–161Google Scholar
- 39.Walpole CS, Bevan S, Bovermann G, Boelsterli JJ, Breckenridge R, Davies JW, Hughes GA, James I, Oberer L, Winter J, et al (1994) The discovery of capsazepine, the first competitive antagonist of the sensory neuron excitants capsaicin and resiniferatoxin. J Med Chem 37:1942–1954PubMedCrossRefGoogle Scholar
- 48.Sontag SJ (1997) Gastroesophageal reflux and asthma. Am J Med 103:84S-90SGoogle Scholar