Psychophysical and electrophysiological studies indicated that the umami substances have no enhancing activity on other primary tastes. Experiments using amiloride clearly show that the umami component of canine chorda tympani nerve response to umami substances is independent of the salt component. Single fiber analysis of the responses of the mouse glossopharyngeal nerve and the monkey primary taste cortex neuron show that the responses to umami substances are independent of other primary tastes. A large synergism between monosodium glutamate (MSG) and disodium 5'‐inosinate (IMP) or disodium 5′‐guanylate (GMP) is observed in dogs and is explained in terms of allosteric effect. The order of intensity of umami taste induced by a mixture of 0.5 mM GMP and 1.5 mM of various agonists for the glutamate receptors was glutamate>ibotenate>dl(+)‐2‐amino‐4‐phosphonobutyric acid (DL‐AP4)‐(+)‐1‐aminocyclopentane‐trans‐1,3‐dicarboxylic acid (trans‐ACPD). Kainate, N‐methyl‐d‐aspartate (NMDA) and (RS)‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA), which are agonists for ionotropic receptors, have no umami taste. It was concluded that the umami receptor is not identical to any of known glutamate receptors, and there seems to be a unique receptor for umami.