The
tachykinins,
substance P,
neurokinin A and
neurokinin B, are a family of
neuropeptides widely distributed in the mammalian central and peripheral nervous system. In the peripheral nervous system,
tachykinins released from peripheral endings of sensory nerves are responsible for the
neurogenic inflammation phenomenon. In the spinal cord/central nervous system,
tachykinins play a role in
pain transmission/perception and in some autonomic reflexes and behaviors. Their actions are mediated by three distinct receptors, termed NK1, NK2 and NK3. All
tachykinin receptors belong to the superfamily of
G protein-coupled receptors, with seven putative transmembrane spanning segments. In the past few years, a number of potent and selective antagonists, of both
peptide and nonpeptide nature, has been developed for the NK1, NK2 and NK3 receptors. The contemporary isolation and cloning of the three
tachykinin receptors enable now to study the molecular determinants for the interaction of natural
tachykinins with their receptors, and the mechanism by which the antagonists interfere in this process. Furthermore, the introduction of
tachykinin antagonists has revealed a striking species-related heterogeneity among the
tachykinin receptors, and has also suggested a possible intra-species heterogeneity for both NK1 and NK2 receptors. However, molecular biology studies are needed to prove the existence of true
tachykinin receptor subtypes.