Takashi Yamamoto, Noritaka Sako and Kenichi Tokita


Umami is a Japanese word introduced by Ikeda in 1909 referring to the taste of monosodium glutamate (MSG), an essential taste effect of sea tangle which has been traditionally used in Japanese cuisine. It is accepted that umami is a unique taste independent of the classical four basic taste qualities. Nucleic acid derivatives such as inosine monophosphate (IMP) are also known as umami substances. Synergism, an enhancement of umami, occurs when MSG is mixed with IMP.The uniqueness of the taste of umami substances and the degree of synergism differ greatly among species of animals. Our previous study showed that rats could not discriminate between the taste of umami substances and sweet-tasting substances. We have also found that the chorda tympani plays a major role in mediating the taste of umami substances, followed by the greater superficial petrosal nerve, and the glossopharyngeal nerve has only a minor role. We recorded chorda tympani responses of rats and obtained the following results. L-AP4, an agonist for mGluR4, showed synergistic effects like MSG when mixed with IMP. MAP4, an antagonist for mGluR4, did not suppress the responses to L-AP4 and the mixture of L-AP4 and IMP. Gurmarin, an anti-sweet peptide, and pronase E, a proteolytic enzyme, suppressed the responses to the mixture of MSG and IMP and the mixture of L-AP4 and IMP. Although no synergism occurred for the mixtures of MSG and sweet substances, the responses to the mixtures of L-AP4 and sweet substances were synergistically enhanced, but they were not suppressed by MAP4, gurmarin or pronase E. On the basis of these response characteristics to umami substances, we have proposed multiple transduction mechanisms for umami taste in rat taste cells.

Alexander A. Bachmanov and Gary K. Beauchamp


Inbred strains of mice provide a powerful tool for genetic dissection of quantitative behavioral traits. We have investigated intake of the umami-tasting substances monosodium glutamate (MSG) and inosine 5′-monophosphate (IMP) in inbred mice. Studies with two inbred strains, C57BL/6ByJ and 129P3/J have revealed strain differences in voluntary consumption of 300 mM MSG which depend, at least partially, on postingestive effects of solution consumption, as well as on strain differences in preferences for much lower MSG concentrations, which depend on perception. The strain difference in MSG acceptance was in the opposite direction to the strain difference in NaCl acceptance and was unrelated to sweetener preference in the F2 generation. Thus, the strain differences in MSG acceptance are not related to the strain differences in salty or sweet taste responsiveness and most likely represent specific umami taste responsiveness. High acceptance of MSG solutions by the C57BL/6ByJ mice was inherited as a recessive trait in the F2 hybrid generation. Further genetic linkage analyses using the F2 hybrids are being conducted to map chromosomal locations of genes determining the strain difference in MSG acceptance. At the same time, a wider range of inbred strains is being phenotyped in a search for new model systems for studying umami substance acceptance.

Kumiko Sugimoto, Kiyohito Nakashima, Keiko Yasumatsu, Kazushige Sasamoto and Yuzo Ninomiya


In order to clarify the role of group III metabotropic glutamate receptor (including mGluR4) in transduction for umami taste, we investigated the effects of monosodium glutamate (MSG) and 2-amino-4-phosphonobutyrate (L-AP4), a mGluR4 agonist, on taste cells by use of electrophysiological and biochemical methods, and Ca2+ imaging in C57BL mice. The responses of the chorda tympani (CT) nerve to MSG were suppressed by gurmarin, a sweet response inhibitor, indicating that the MSG response may be partly mediated by sweet receptors, while the CT responses to L-AP4 and the glossopharyngeal (GL) nerve responses to MSG were little suppressed by gurmarin suggesting that these responses may be mediated by only umami receptors. Biochemical study demonstrated that MSG stimulation significantly elevated both adenosine 3′, 5′-cyclic monophosphate (cAMP) and inositol 1,4,5-triphosphate (IP3) levels in the fungiform papillae. The increase in cAMP might occur through sweet receptors, which is consistent with CT nerve responses. The increase in IP3 levels may relate to intracellular events mediated by group III mGluRs, because MSG and L-AP4 induced increment of intracellular Ca2+ concentration in some taste cells. Whole-cell patchclamp recording from isolated taste cells showed that L-AP4 induced not only outward currents with a conductance decreases but also inward currents with conductance increases at about resting potentials. These inward currents reversed at +10-+30 mV suggesting that cation conductance was activated by L-AP4. These results strongly support the idea that phospholipase C activation mediated by group III mGluRs is involved in transduction mechanism for umami taste, and also suggest the possibility that stimulation of the mGluRs may cause activation of cation conductance as well as [Ca2+]i elevation.

E.T. Rolls

Thomas R. Scott, Justus V. Verhagen, Barbara K. Giza, Zoltan Karádi and Yutaka Oomura


The issue that has divided opinion over the status of umami as a basic taste quality is its relationship with the taste of sodium salt. That is addressed here, informed by electrophysiological data from the hindbrain of rats and from the forebrain of macaques. In multidimensional spaces, generated from patterns of neural activity evoked in the rat's hindbrain by an array of taste stimuli, MSG does indeed lie near the position of NaCl. Yet when sodium transduction is disrupted by the lingual application of amiloride, the impact on the taste response to MSG is minor, and the pattern of activity it elicits is unaltered. Thus, MSG generates a taste quality that transcends saltiness, one that survives even as saltiness is compromised. This conclusion is in accord with the independent transduction mechanisms ascribed to MSG. In the macaque's taste system, MSG is an effective stimulus with a dynamic range of 0.009 to 0.300 M. Approximately one-third of the taste cells at each synaptic relay respond to MSG at 0.1 M. MSG evoked a neural response profile in primary taste cortex that correlated quite well with that elicited by NaCl, in accord with the pronounced salty component humans report for its taste. At succeeding synaptic relays, however, that relationship deteriorated, becoming increasingly distant and labile. At higher-order gustatory levels, MSG evoked a profile that was no more similar to those of the basic stimuli than they are to each other. This implies that MSG warrants independent status as a basic taste stimulus, serving as the prototype for the umami quality.

Seong-Hee Oh, Yukako Hayashi, Keiko Iseki, Diego Restrepo, John Teeter and Tomohiko Mori


We have previously reported that monosodium glutamate (MSG) stimulation elicited three types responses (transient inward current, sustained inward current and outward current) while L-AP4 (a potent mGluR4 agonist) evoked only outward currents in C57BL/6J mouse taste cells. The outward current responses to MSG and L-AP4 appeared to be mediated by metabotropic glutamate type 4 receptors (mGluR4). In this study, we examined whether agonists of ionotropic glutamate receptor agonists (NMDA, AMPA and ibotenic acid) also elicit responses in mouse taste cells. NMDA (1 mM) elicited transient inward currents, similar to those often observed with MSG, indicating the presence of NMDA receptor/channels that are permeable to Ca2+ ions and are activated by MSG in some taste cells. The sustained inward current response to MSG appeared to result from activation of a nonselective cation conductance, but it is not known if this response is coupled to ionotropic or metabotropic receptors. AMPA (1 mM) elicited small outward currents in all responding cells. Ibotenic acid, which produces a considerably stronger umami taste than MSG in humans, elicited two types of responses in isolated cells; transient inward currents and sustained inward current, suggesting that inward, as well as outward, currents are related to umami transduction. Also, we confirmed that MSG, AP4 (2 mM) and NMDA all can increase [Ca2+]i in taste cells. These results indicate that some cells have both metabotropic and ionotropic receptors, while other taste cells have only one or the other type of receptor.

Edmund T. Rolls


To investigate the neural encoding of glutamate (umami) taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex (secondary) taste area. First, it was shown that there is a representation of the taste of glutamate which is separate from the representation of the other prototypical tastants sweet (glucose), salt (NaCl), bitter (quinine) and sour (HCl). Second, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. Third, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5′-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Fourth, concentration-response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioural satiety, revealing a mechanism of satiety. In some cases this reduction was sensory-specific. Sixth, it was shown in psychophysical experiments in humans that the flavor of umami is strongest with a combination of corresponding taste and olfactory stimuli (e.g. monosodium glutamate and garlic odor). The hypothesis is proposed that part of the way in which glutamate works as a flavor enhancer is by acting in combination with corresponding food odors. The appropriate associations between the odor and the glutamate taste may be learned at least in part by olfactory to taste association learning in the primate orbitofrontal cortex. Seventh, in neuroimaging experiments with functional magnetic resonance imaging (fMRI) in humans, it was shown that in humans umami taste produced by monosodium glutamate or by inosine monophosphate produced activation in a region of the anterior insula which is the putative human primary taste cortex and in a part of the orbitofrontal cortex which is the putative human secondary taste cortex.

Keiko Iseki, Yukako Hayashi, Seong-Hee Oh, John Teeter, Diego Restrepo and Tomohiko Mori


Monosodium glutamate (MSG) elicits a unique taste in humans called 'umami' that is potentiated synergistically by the 5′-ribonucleotides IMP and GMP.Recent studies suggest that several mechanisms are involved in the transduction of umami taste. We have previously shown that MSG (10 mM) induced three different responses in mouse taste cells under whole-cell voltage-clamp in Na+ free Ringer solution; transient inward current, sustained inward current and outward current. Two, and occasionally all three types of currents, were observed in the same cell. We report here responses of mouse taste cells to the metabotropic glutamate receptor agonist, L-AP4 (1 mM), a mixture of MSG (10 mM) and IMP (0.5 mM), and a mixture of L-AP4 (1 mM) and IMP (0.5 mM) under whole-cell voltage-clamp. The mixture of MSG and IMP induced three different types of responses, similar to MSG alone. But the amplitudes of both the transient and sustained inward currents were larger than observed with MSG alone. The outward currents were similar in amplitude to those elicited by MSG alone. L-AP4 induced only outward currents in taste cells, while the mixture of L-AP4 and IMP induced both sustained inward currents and outward currents. These results suggest that umami taste reception may involve the coactivation of mGluR4 and one or more types of ionotropic glutamate receptors. Presumably the net transduction current resulting from activation of these receptors mediates the umami taste response, while an additional receptor or receptor site which is related to sustained inward current response, is involved in the synergistic effect of ribonucleotides.

Nirupa Chaudhari


Monosodium L-glutamate (MSG), a natural component of many foods, is an important gustatory stimulus that elicits a taste quality called umami. In addition to being a potent taste stimulus, glutamate also may be a neurotransmitter at tastebud synapses. In mammalian taste buds, molecular, physiological and behavioral evidence has accumulated for the presence of ion channels gated by glutamate as well as metabotropic (G protein coupled) receptors for glutamate. Some of these may represent umami taste receptor(s), while others function to detect synaptic glutamate. To identify which glutamate receptors, if any, play a role in taste transduction, it is critical to determine if their functional properties are consistent with key features of umami taste. We have recently cloned a novel variant of the metabotropic glutamate receptor 4 (mGluR4). In situ hybridization shows that the gene is expressed in a subset of circumvallate and foliate taste buds in the rat. The variant mGluR4 contains a truncated extracellular N-terminus that dramatically alters the putative binding site for glutamate. We have functionally expressed this receptor in CHO cells, and demonstrated that it responds to glutamate. The receptor couples negatively to a cAMP cascade and displays a distinctive concentration-response relationship for glutamate, with a threshold similar to the taste threshold for MSG. Importantly, the receptor is also activated by L-AP4, a compound that mimics the taste of MSG in rats and in humans. We have termed the novel receptor taste-mGluR4. The similarities of its properties to MSG taste suggests that taste-mGluR4 is a taste receptor for glutamate.

Jun Hara, Hirotaka Hara, Dale Martin, Xiangdong Chen, Jershonda F. Hartsfield and Cesar D. Fermin

Joseph C. Holt, Paul S. Guth, Paola Perin and Charles A. Norris

Graciela Meza

Alfons Rüsch, Jeffrey R. Holt, Ruth Anne Eatock and Melissa A. Vollrath

Stephen J. Warner, Margaret I. Lomax, Cagri G. Besirli and Tzy-Wen L. Gong

Péter Sántha, Ferenc Domoki, Anna Juhász, Mária Dux and Gábor Jancsó

Jean-Jacques Puizillout, Xinhuai Liu and Fabienne Martini-Luccarini

R. C. Peters, D. A. Kraaij and F. Bretschneider

Donald Ganchrow, Gadi Pelled and Judith R. Ganchrow

I. Nagy, P. Szücs, L. Urban, E. Polgár, J. Croxford and A. Dray

John Bradshaw and Lesley Rogers

On the cutting edge of neuropsychology and cognitive science, this book investigates lateral asymmetries in the human brain and contrasts these with asymmetries in primates as well as invertebrates, primitive vertebrates, birds, and other mammals. Nine illustrated chapters present asymmetries in lower life forms, progress to hominoids and hominids, and discuss how such asymmetries are responsible for the development of language, upright posture, tool use, intellect, and self-awareness in humans. A summary and conclusions section at the end of each chapter provide both a general survey and a balanced judgment of any controversial aspects previously discussed. Regarded as experts in their field, the authors have received much acclaim for their previous books.Key Features -- Shows that lateralization of function occurs systematically throughout the animal kingdom and is not unique to humans -- Explains why lateralization of function depends upon a complex interplay of generic, structural, and environmental factors and is also subject to hormonal and maturational determination -- Demonstrates the close commonality between human and nonhuman species with respect to such hitherto uniquely human attributes as consciousness, tool use, and language -- Provides an account of human evolution in the context of language, tool use, art, and intellect at the neurological, behavioral, and archaeological levels -- a new synthesis

Edited by Medvedev

Proceedings Paleopathology Association

4th European meeting Middelburg/Antwerpen, 15-19 September 1982

Edited by Haneveld and Perizonius

Mammal collector's manual

A guide for collecting, documenting and preparing mammal specimens




(Fossils of Ontario,1)




Essays on Palaeontology in honour of Loris Shano Russell



From 2006 Gene Therapy and Regulation is no longer published by Brill. Please contact the Editor-in-Chief: Roger Bertolotti, Ph. D., Gene Therapy and Regulation Research Faculty of Medicine, University of Nice Sophia Antipolis, Avenue de Valombrose, 06107 Nice, France (Tel: +33 4 9381 7381, Fax: +33 4 9331 7253, E-mail: Roger Bertolotti).
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Sensory Neuron

The International Interdisciplinary Journal Reporting Basic and Clinical Research on Sensory Receptors and Primary Afferent Neurons