Adenosine Enhances Sweet Taste through A2B Receptors in the Taste Bud

Dando, Robin; Dvoryanchikov, Gennady; Pereira, Elizabeth; Chaudhari, Nirupa; Roper, Stephen D.

doi:10.1523/jneurosci.4070-11.2012

Cited by 74 publications

(73 citation statements)

References 55 publications

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“…43 Upon secretion, ATP acts as a neurotransmitter on nearby sensory afferent fibers 44,45 ; ATP also acts as a paracrine/autocrine hormone, binding with receptors expressed on neighboring taste receptor cells. [46][47][48][49][50] Type III cells release serotonin, c-amino butyric acid, and norepinephrine and are most notable for possessing synapses. [51][52][53][54] These cells, also termed presynaptic cells, express voltage-gated calcium channels associated with neurotransmitter release, enzymes for serotonin, and c-amino butyric acid, as well as uptake transporters for biogenic amines.…”

Section: Taste Bud Anatomy and Physiologymentioning

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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Section: Taste Bud Anatomy and Physiologymentioning

confidence: 99%

Taste perception, associated hormonal modulation, and nutrient intake

et al. 2015

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“…One microgram of extracted total RNA was reverse transcribed at 37°C using Omniscript reverse transcriptase (Qiagen, Valencia, CA), and 2 l of mixture was taken for subsequent PCR. The following primers were used to detect the A 2AR (20): sense, 5=-cctgaattccactccggtaca-3=; antisense, 5=-cagttgttccagcccagcat-3=. The following primers were used to detect the A2BR (20): sense, 5=-tcttcctcgcctgcttcgt-3=; antisense, 5=-ccagtgaccaaacctttatacctga-3=.…”

Section: Jg Cell Adenosine Receptor Expressionmentioning

confidence: 99%

“…The following primers were used to detect the A 2AR (20): sense, 5=-cctgaattccactccggtaca-3=; antisense, 5=-cagttgttccagcccagcat-3=. The following primers were used to detect the A2BR (20): sense, 5=-tcttcctcgcctgcttcgt-3=; antisense, 5=-ccagtgaccaaacctttatacctga-3=. Primer pairs for each transcript were designed to span an exon-intron-exon boundary (4).…”

Section: Jg Cell Adenosine Receptor Expressionmentioning

confidence: 99%

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Adenosine inhibits renin release from juxtaglomerular cells via an A₁ receptor-TRPC-mediated pathway

Ortiz-Capisano

Atchison

Harding

et al. 2013

American Journal of Physiology-Renal Physiology

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Ortiz-Capisano MC, Atchison DK, Harding P, Lasley RD, Beierwaltes WH. Adenosine inhibits renin release from juxtaglomerular cells via an A 1 receptor-TRPC-mediated pathway. Am J Physiol Renal Physiol 305: F1209 -F1219, 2013. First published July 24, 2013 doi:10.1152/ajprenal.00710.2012.-Renin is synthesized and released from juxtaglomerular (JG) cells. Adenosine inhibits renin release via an adenosine A 1 receptor (A1R) calcium-mediated pathway. How this occurs is unknown. In cardiomyocytes, adenosine increases intracellular calcium via transient receptor potential canonical (TRPC) channels. We hypothesized that adenosine inhibits renin release via A 1R activation, opening TRPC channels. However, higher concentrations of adenosine may stimulate renin release through A 2R activation. Using primary cultures of isolated mouse JG cells, immunolabeling demonstrated renin and A 1R in JG cells, but not A2R subtypes, although RT-PCR indicated the presence of mRNA of both A 2AR and A2BR. Incubating JG cells with increasing concentrations of adenosine decreased renin release. Different concentrations of the adenosine receptor agonist N-ethylcarboxamide adenosine (NECA) did not change renin. Activating A 1R with 0.5 M N6-cyclohexyladenosine (CHA) decreased basal renin release from 0.22 Ϯ 0.05 to 0.14 Ϯ 0.03 g of angiotensin I generated per milliliter of sample per hour of incubation (AngI/ml/mg prot) (P Ͻ 0.03), and higher concentrations also inhibited renin. Reducing extracellular calcium with EGTA increased renin release (0.35 Ϯ 0.08 g AngI/ml/mg prot; P Ͻ 0.01), and blocked renin inhibition by CHA (0.28 Ϯ 0.06 g AngI/ml/mg prot; P Ͻ 0. 005 vs. CHA alone). The intracellular calcium chelator BAPTA-AM increased renin release by 55%, and blocked the inhibitory effect of CHA. Repeating these experiments in JG cells from A 1R knockout mice using CHA or NECA demonstrated no effect on renin release. However, RT-PCR showed mRNA from TRPC isoforms 3 and 6 in isolated JG cells. Adding the TRPC blocker SKF-96365 reversed CHA-mediated inhibition of renin release. Thus A 1R activation results in a calcium-dependent inhibition of renin release via TRPC-mediated calcium entry, but A 2 receptors do not regulate renin release. renin; adenosine; calcium; A 1R; CHA; adenosine receptors; transient receptor potential canonical RENIN IS PRODUCED BY, STORED in, and released from juxtaglomerular (JG) cells located in the lamina media of the afferent arteriole at the entrance to the glomerulus (7, 31). Two main intracellular second-messenger systems are known to regulate renin secretion: stimulation of renin release by the cyclic nucleotide cAMP; and inhibition or renin secretion by increased intracellular calcium (1-3, 16, 25, 30).Adenosine is a purine nucleoside catabolite of ATP. Adenosine's effects are mediated by the activation of four G protein-coupled receptor (GPCR) subtypes: A 1 , A 2A , A 2B , and A 3 (13, 44). Adenosine inhibits renin secretion in vivo and in vitro (9, 37). It is considered that adenosine from the macula densa inhib...

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“…As a practical consideration, many laboratories, including our own, rely on protease isolation of taste buds from a peeled epithelium (8,9,22). Lingual epithelium containing taste buds is typically detached from underlying stroma with an initial collagenase digestion before it is peeled.…”

Section: Resultsmentioning

confidence: 99%

A permeability barrier surrounds taste buds in lingual epithelia

Dando

Pereira

Kurian

et al. 2015

American Journal of Physiology-Cell Physiology

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Epithelial tissues are characterized by specialized cell-cell junctions, typically localized to the apical regions of cells. These junctions are formed by interacting membrane proteins and by cytoskeletal and extracellular matrix components. Within the lingual epithelium, tight junctions join the apical tips of the gustatory sensory cells in taste buds. These junctions constitute a selective barrier that limits penetration of chemosensory stimuli into taste buds (Michlig et al. J Comp Neurol 502: 1003–1011, 2007). We tested the ability of chemical compounds to permeate into sensory end organs in the lingual epithelium. Our findings reveal a robust barrier that surrounds the entire body of taste buds, not limited to the apical tight junctions. This barrier prevents penetration of many, but not all, compounds, whether they are applied topically, injected into the parenchyma of the tongue, or circulating in the blood supply, into taste buds. Enzymatic treatments indicate that this barrier likely includes glycosaminoglycans, as it was disrupted by chondroitinase but, less effectively, by proteases. The barrier surrounding taste buds could also be disrupted by brief treatment of lingual tissue samples with DMSO. Brief exposure of lingual slices to DMSO did not affect the ability of taste buds within the slice to respond to chemical stimulation. The existence of a highly impermeable barrier surrounding taste buds and methods to break through this barrier may be relevant to basic research and to clinical treatments of taste.

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Adenosine Enhances Sweet Taste through A2B Receptors in the Taste Bud

Cited by 74 publications

References 55 publications

Taste perception, associated hormonal modulation, and nutrient intake

Taste perception, associated hormonal modulation, and nutrient intake

Adenosine inhibits renin release from juxtaglomerular cells via an A₁ receptor-TRPC-mediated pathway

A permeability barrier surrounds taste buds in lingual epithelia

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Adenosine Enhances Sweet Taste through A2B Receptors in the Taste Bud

Cited by 74 publications

References 55 publications

Taste perception, associated hormonal modulation, and nutrient intake

Taste perception, associated hormonal modulation, and nutrient intake

Adenosine inhibits renin release from juxtaglomerular cells via an A1 receptor-TRPC-mediated pathway

A permeability barrier surrounds taste buds in lingual epithelia

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Adenosine inhibits renin release from juxtaglomerular cells via an A₁ receptor-TRPC-mediated pathway