Mayu Niki

Modulation of sweet responses of taste receptor cells

Taste receptor cells play a major role in detection of chemical compounds in the oral cavity. Information derived from taste receptor cells, such as sweet, bitter, salty, sour and umami is important for evaluating the quality of food components. Among five basic taste qualities, sweet taste is very attractive for animals and influences food intake. Recent studies have demonstrated that sweet taste sensitivity in taste receptor cells would be affected by leptin and endocannabinoids. Leptin is an anorexigenic mediator that reduces food intake by acting on leptin receptor Ob-Rb in the hypothalamus. Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known as orexigenic mediators that act via cannabinoid receptor 1 (CB1) in the hypothalamus and limbic forebrain to induce appetite and stimulate food intake. At the peripheral gustatory organs, leptin selectively suppresses and endocannabinoids selectively enhance sweet taste sensitivity via Ob-Rb and CB1 expressed in sweet sensitive taste cells. Thus leptin and endocannabinoids not only regulate food intake via central nervous systems but also modulate palatability of foods by altering peripheral sweet taste responses. Such reciprocal modulation of leptin and endocannabinoids on peripheral sweet sensitivity may play an important role in regulating energy homeostasis.

Reciprocal Modulation of Sweet Taste by Leptin and Endocannabinoids

Sweet taste perception is important for animals to detect carbohydrate source of calories and has a critical role in the nutritional status of animals. Recent studies demonstrated that sweet taste responses can be modulated by leptin and endocannabinoids [anandamide (N-arachidonoylethanolamine) and 2-arachidonoyl glycerol]. Leptin is an anorexigenic mediator that reduces food intake by acting on hypothalamic receptor, Ob-Rb. Leptin is shown to selectively suppress sweet taste responses in wild-type mice but not in leptin receptor-deficient db/db mice. In marked contrast, endocannabinoids are orexigenic mediators that act via CB(1) receptors in hypothalamus and limbic forebrain to induce appetite and stimulate food intake. In the peripheral taste system, endocannabinoids also oppose the action of leptin and enhance sweet taste sensitivities in wild-type mice but not in mice genetically lacking CB(1) receptors. These findings indicate that leptin and endocannabinoids not only regulate food intake via central nervous systems but also may modulate palatability of foods by altering peripheral sweet taste responses via their cognate receptors.

Modulation of sweet taste sensitivities by endogenous leptin and endocannabinoids in mice

Potential roles of endogenous leptin and endocannabinoids in sweet taste were examined by using pharmacological antagonists and mouse models including leptin receptor deficient (db/db) and diet‐induced obese (DIO) mice. Chorda tympani (CT) nerve responses of lean mice to sweet compounds were increased after administration of leptin antagonist (LA) but not affected by administration of cannabinoid receptor antagonist (AM251). db/db mice showed clear suppression of CT responses to sweet compounds after AM251, increased endocannabinoid levels in the taste organ, and enhanced expression of a biosynthesizing enzyme of endocannabinoids in taste cells. The effect of LA was gradually decreased and that of AM251 was increased during the course of obesity in DIO mice. These findings suggest that circulating leptin, but not local endocannabinoids, is a dominant modulator for sweet taste in lean mice and endocannabinoids become more effective modulators of sweet taste under conditions of deficient leptin signalling.

Humoral modulation of sweet taste sensitivities for energy homeostasis

freezing behavior among a pair of odorant molecules, which had identical chemical compositions but had different steric structures. In our screening experiments, a majority of odorant receptors were commonly activated by both fear-odors and no-fear-odors, which have identical functional groups and have closely related chemical compositions. However, we have identified a small number of odorant receptors, which were activated by the multiple fear-odors, but not by no-fear-odors that had closely related chemical structures with the fear-odors. In this symposium, we will discuss about the relationships among fear-odors, fear-receptors, and fear responses. Mice can learn to associate an odorant molecule with an electrical shock to induce learned-freezing behavior. We compared physiological responses and neuronal activities in innate-freezing mice to those in learned-freezing mice. As a result, we have found that particular physiological responses and activation patterns of the neuronal circuits in the specific area in the brain were totally different between mice, which demonstrate innate and learned freezing behaviors. These results suggest that there are at least two distinct states of fear in the mice brain.

Reception and Transmission of Taste Information in Type II and Type III Taste Bud Cells

Abstract Gustatory information processing begins with taste bud cells, which are activated by sapid molecules via specific taste receptors and transmit their signals to gustatory afferent fibers. Taste bud cells are morphologically classified into 4 groups (Type I – IV cells), two of which are involved in gustatory signaling. Type II cells express sweet, bitter, and umami taste receptors and transduction components and respond best to sweet, bitter, or umami stimuli, suggesting that sweet, bitter, and umami tastes are detected by different sets of Type II cells. Type III cells express putative sour taste receptors and respond to sour or multiple taste stimuli, indicating that sour tastes are mediated by Type III cells. These data suggest that each taste quality could be discriminated among taste bud cells. Type II cells do not possess a conventional synaptic structure but they release ATP in response to taste stimuli. Type III cells have a synaptic structure and they release serotonin and norepinephrine but not ATP. Therefore, each taste cell may use distinct mechanisms and transmitters for signal transmission to gustatory nerve fibers.