Expression and Physiological Actions of Cholecystokinin in Rat Taste Receptor Cells

Herness, Scott; Zhao, Fuqing; Lu, Shicheng; Kaya, Namik; Shen, Tiansheng

doi:10.1523/jneurosci.22-22-10018.2002

Cited by 103 publications

(99 citation statements)

References 54 publications

(60 reference statements)

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“…To date, leptin (9-11), CCK (31,32), VIP (32), NPY (33), and GLP-1 (13) are implicated in the modulation of peripheral taste sensitivity. Leptin and GLP-1 are known to be modulators for sweet taste.…”

Section: Resultsmentioning

confidence: 99%

Endocannabinoids selectively enhance sweet taste

Yoshida

Ohkuri

Jyotaki

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

172

162

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Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known orexigenic mediators that act via CB 1 receptors in hypothalamus and limbic forebrain to induce appetite and stimulate food intake. Circulating endocannabinoid levels inversely correlate with plasma levels of leptin, an anorexigenic mediator that reduces food intake by acting on hypothalamic receptors. Recently, taste has been found to be a peripheral target of leptin. Leptin selectively suppresses sweet taste responses in wild-type mice but not in leptin receptor-deficient db/db mice. Here, we show that endocannabinoids oppose the action of leptin to act as enhancers of sweet taste. We found that administration of AEA or 2-AG increases gustatory nerve responses to sweeteners in a concentration-dependent manner without affecting responses to salty, sour, bitter, and umami compounds. The cannabinoids increase behavioral responses to sweet-bitter mixtures and electrophysiological responses of taste receptor cells to sweet compounds. Mice genetically lacking CB 1 receptors show no enhancement by endocannnabinoids of sweet taste responses at cellular, nerve, or behavioral levels. In addition, the effects of endocannabinoids on sweet taste responses of taste cells are diminished by AM251, a CB 1 receptor antagonist, but not by AM630, a CB 2 receptor antagonist. Immunohistochemistry shows that CB 1 receptors are expressed in type II taste cells that also express the T1r3 sweet taste receptor component. Taken together, these observations suggest that the taste organ is a peripheral target of endocannabinoids. Reciprocal regulation of peripheral sweet taste reception by endocannabinoids and leptin may contribute to their opposing actions on food intake and play an important role in regulating energy homeostasis.energy homeostasis | gustation | reciprocal regulation E ndocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known orexigenic mediators that act via CB 1 receptors in hypothalamus and limbic forebrain to induce appetite (1, 2) and stimulate food intake (3). Systemic administration of exogenous cannabinoids or endocannabinoids in rodents causes hyperphagia (4) and increases the preference for palatable substances such as sucrose solution or food pellets (5, 6). These effects are mediated by the CB 1 receptor: pretreatment with the CB 1 antagonist SR141716 inhibited hyperphagia and reduced consumption of both bland and palatable foods (4-6). The natural "liking" reactions of rats to sweet compounds were amplified by endogenous cannabinoid signals in nucleus accumbens (7). Thus, endocannabinoids may be related to hedonic aspects of sweet taste.There is growing evidence that taste function can be modulated by hormones or other factors that act on receptors present in the peripheral gustatory system. Leptin, an anorexigenic mediator that reduces food intake by acting on hypothalamic receptors (8), selectively suppresses sweet taste responses and th...

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Section: Resultsmentioning

confidence: 99%

Endocannabinoids selectively enhance sweet taste

Yoshida

Ohkuri

Jyotaki

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

172

162

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“…Hormones that bind to receptors on taste cells alter the palatability of food and, therefore, intake. Current knowledge of the hormonal modulation of taste function is summarized in Table 1 [60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][77] and described in greater detail below.…”

Section: Hormonal Modulation Of Taste Functionmentioning

confidence: 99%

“…85,86 Research suggests that centrally expressed CCK may also contribute to the sensation of satiety. [87][88][89] Herness et al 65 were the first to localize the peptide CCK and its receptor, CCK-A, to subsets of taste receptor cells. It was determined that the CCK receptor is completely coexpressed in CCKpositive taste cells, suggesting an autocrine mechanism of CCK action in taste cells.…”

Section: Cholecystokininmentioning

confidence: 99%

Taste perception, associated hormonal modulation, and nutrient intake

et al. 2015

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It is well known that taste perception influences food intake. After ingestion, gustatory receptors relay sensory signals to the brain, which segregates, evaluates, and distinguishes the stimuli, leading to the experience known as "flavor." It is well accepted that five taste qualities -sweet, salty, bitter, sour, and umami -can be perceived by animals. In this review, the anatomy and physiology of human taste buds, the hormonal modulation of taste function, the importance of genetic chemosensory variation, and the influence of gustatory functioning on macronutrient selection and eating behavior are discussed. Individual genotypic variation results in specific phenotypes of food preference and nutrient intake. Understanding the role of taste in food selection and ingestive behavior is important for expanding our understanding of the factors involved in body weight maintenance and the risk of chronic diseases including obesity, atherosclerosis, cancer, diabetes, liver disease, and hypertension.

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“…Patch clamp experiments were performed on TRCs dissociated from CV and FOL as previously described (5,10). Chloride or KIR currents were isolated as previously described (7,17).…”

Section: Rt-pcrmentioning

confidence: 99%

“…A number of neurotransmitters, neuropeptides, and their corresponding receptors form intricate hard-wired pathways in the bud for information processing. Some examples of cell-to-cell communication in the taste bud include serotonin (5,6), norepinephrine (7,8), ATP (9), cholecystokinin (10), and neuropeptide Y (11). It is believed that activation of TRCs results in information processing within the bud and ultimate activation of the afferent nerve fibers.…”

mentioning

confidence: 99%

GABA expression in the mammalian taste bud functions as a route of inhibitory cell-to-cell communication

Cao

Zhao

Kolli

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

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Recent advances have underscored cell-to-cell communication as an important component of the operation of taste buds with individual taste receptor cells (TRCs) communicating with oneanother by means of a number of neurotransmitters and neuropeptides, although functional roles are not yet understood. Here, we characterize the presence, distribution pattern, phenotype, and functional consequences of a previously undescribed inhibitory route within the taste bud mediated by the classic neurotransmitter GABA and its receptors. By using immunocytochemistry, subsets of TRCs within rat taste buds were identified as expressing GABA, and its synthetic enzyme glutamate decarboxylase (GAD). GAD expression was verified with Western blotting. Immunofluorescent studies revealed complex coexpression patterns of GAD with the TRC protein markers gustducin, neural cell adhesion molecule, protein gene product 9.5, and synaptosomal-associated protein of 25 kDa that collectively outline hardwired signaling pathways of GABAergic TRCs. RT-PCR and immunocytochemistry demonstrated that both GABA A and GABAB receptors are expressed in the taste bud. The later was observed in a subset TRCs paracrine to GAD-expressing TRCs. Physiological effects of GABA were examined by patch clamp recordings. GABA and the GABAA agonists muscimol and isoguvacine enhanced isolated chloride currents in a dose-dependent manner. Also, GABA and the GABAB agonist baclofen both elicited increases of the inwardly rectifying potassium currents that could be blocked by the GABAB receptor antagonist CGP 35348 and the G protein blocker GDP-␤S. Collectively, these data suggest that GABAergic TRCs are able to shape the final chemosensory output of the bud by means of processes of cell-to-cell modulation.gustation ͉ neuromodulation ͉ neurotransmitters ͉ transduction ͉ paracrine signaling R ecent studies of gustatory transduction (1, 2) have dramatically altered our understanding of how the taste bud operates. Early views of taste-bud function were based on anatomical studies and classified taste receptor cells (TRCs) into types I, II, or III. Type III cells are synaptically connected to afferent nerve fibers and were considered as ''true'' receptor cells, because they communicate directly with the central nervous system. Types I and II, differing in their opacity (dark or light, respectively) lack synapses, and were considered supportive cells. The discovery of the 7 transmembrane receptor families T1R and T2R and other downstream signaling molecules in type II cells changed the view that single TRCs operate in isolation but instead function collectively through cell-to-cell communication in producing the neural output (3, 4). The notion has lead to discussing transduction as early, or primary, events leading to activation of late, or secondary, events. Early events involve steps leading to the activation (i.e., depolarization) of an individual TRC. Tastant molecules interact with receptors of the T1R or T2R families in type II cells or with ion channels such as the trp...

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Expression and Physiological Actions of Cholecystokinin in Rat Taste Receptor Cells

Cited by 103 publications

References 54 publications

Endocannabinoids selectively enhance sweet taste

Endocannabinoids selectively enhance sweet taste

Taste perception, associated hormonal modulation, and nutrient intake

GABA expression in the mammalian taste bud functions as a route of inhibitory cell-to-cell communication

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