Interaction of Saliva and Taste

Spielman, Andrew I.

doi:10.1177/00220345900690030101

Cited by 150 publications

(91 citation statements)

References 62 publications

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“…For example, all of the PD patients in our study were on antiparkinsonian medications, which have been described to be able to induce alteration in taste function or dry mouth [1]. Poor oral hygiene or changes in salivary consistency in patients with PD are other plausible explanations [18][19][20].…”

Section: Discussionmentioning

confidence: 99%

Taste function in patients with Parkinson disease

et al. 2010

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Despite the important role of taste function in nutrition and health, little is known about changes in taste function caused by Parkinson disease (PD). The taste function of 31 PD patients and 29 healthy controls was assessed quantitatively using filter paper taste strip tests (TSTs) impregnated with four basic taste qualities at four different concentrations. The mean TST score was significantly lower in PD patients, as a consequence of taste impairment in the female PD patients (it did not differ significantly in males), which was likely to be attributable to the lower Mini-Mental State Examination score in patients with PD than in controls in women. TST scores in PD patients were not correlated with patient age, duration, or severity of their PD, or olfactory function. The findings of our study suggest that taste dysfunction should be included in the list of nonmotor symptoms of PD.

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Section: Discussionmentioning

confidence: 99%

Taste function in patients with Parkinson disease

et al. 2010

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“…For instance, we know now that oral intake of monosodium glutamate stimulates exocrine secretion (saliva and gastric, bile, and pancreatic juices) (28,29,33,39,43) as well as the GI endocrine system such as insulin (11). Moreover, the infusion of monosodium glutamate into the stomach directly evokes a gastric vagovagal reflex accompanied by insulin secretion (27).…”

Section: Discussionmentioning

confidence: 99%

Luminal amino acid sensing in the rat gastric mucosa

Uneyama¹,

Niijima²,

Gabriel³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

145

151

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. Luminal amino acid sensing in the rat gastric mucosa. Am J Physiol Gastrointest Liver Physiol 291: G1163-G1170, 2006. First published June 29, 2006 doi:10.1152/ajpgi.00587.2005.-Recent advancements in molecular biology in the field of taste perception in the oral cavity have raised the possibility for ingested nutrients to be "tasted" in the upper gastrointestinal tract. The purpose of this study was to identify the existence of a nutrient-sensing system by the vagus in the rat stomach. Afferent fibers of the gastric branch increased their firing rate solely with the intragastric application of the amino acid glutamate. Other amino acids failed to have the same effect. This response to glutamate was blocked by the depletion of serotonin (5-HT) and inhibition of serotonin receptor 3 (5-HT3) or nitric oxide (NO) synthase enzyme. Luminal perfusion with the local anesthesia lidocaine abolished the glutamate-evoked afferent activation. The afferent response was also mimicked by luminal perfusion with a NO donor, sodium nitroprusside. In addition, the NO donorinduced afferent activation was abolished by 5-HT 3 blockade as well. Altogether, these results strongly suggest the existence of a sensing system for glutamate in the rat gastric mucosa. Thus luminal glutamate would enhance the electrophysiological firing rate of afferent fibers from the vagus nerve of the stomach through the production of mucosal bioactive substances such as NO and 5-HT. Assuming there is a universal coexistence of free glutamate with dietary protein, a glutamate-sensing system in the stomach could contribute to the gastric phase of protein digestion.visceral nutrient sensing; rat vagal gastric afferent; serotonin; nitric oxide THE NUMBER OF ARTICLES DEDICATED to the abdominal vagus nerve that were focused in gut nutrient sensing has increased dramatically over the last decade (33,36,42). This is due to the advancement of techniques that facilitated the study of visceral afferent fibers and their function and characteristic electrophysiological patterns and also due to recognition that these fibers are important for body nutrient homeostasis. Psychophysiological approaches for the understanding of ingestive behavior have demonstrated that the presence of food in the upper gastrointestinal (GI) tract plays a critical role in determining meal size. The vagus nerve is extensively distributed throughout the GI tract, from the posterior region of oral cavity and esophagus to the lowest part of the colon, and functions as the primary neuroanatomical circuit in the gut-brain axis to transmit meal-related signals from the GI mucosa to the central nervous system. This is where regulatory processes (e.g., ingestive behavior, nutrient absorption, GI secretion, and stomach emptying) as well as conscious sensations (e.g., satiety, nausea, and discomfort) take place (5, 22, 37).Recently, it has been shown that taste transduction-related molecules, such as ␣-gustducin and a family of bitter-sensing taste receptors (T 2 Rs), were also expressed at the GI mu...

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“…The peri-receptor milieu of TRCs removes food, permits the solubility of taste substances and their diffusion to taste receptors, and provides a continuously renewed aqueous milieu (Mese and Matsuo 2007). Their morphological and secretory characteristics and their anatomical relationship with taste buds make VEGs important in taste-reception mechanisms Bradley 1987, 1988;Spielman 1990;Matsuo 2000). CP and VEGs have also been hypothesized to constitute a single functional unit of the peripheral taste mechanism, in which TRCs and VEGs represent the chemoreceptive and secretory parts, respectively (Sbarbati et al 1999), a structural organization resembling that of other tissues, such as pancreatic and biliary ducts (Höfer and Drenckhahn 1998).…”

Section: Introductionmentioning

confidence: 99%

Amylase expression in taste receptor cells of rat circumvallate papillae

et al. 2009

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The chemical composition of the luminal content is now accepted to have a profound influence on the performance of chemosensory receptors. Gustatory and intestinal chemoreceptors have in common their expression of molecules involved in taste sensing and signal transduction pathways. The recent finding that enterocytes of the duodenal epithelium are capable of expressing luminal pancreatic amylase suggests that taste cells of the gustatory epithelium might, in the same way, express salivary amylase in the oral cavity. Therefore, we investigated amylase expression in rat circumvallate papillae by using analyses involving immunohistochemistry, Western blot, and reverse transcription with the polymerase chain reaction. In addition, we used double-labeling confocal laser microscopy to compare amylase immunolabeling with that of the following markers: protein gene product 9.5 (PGP 9.5) and chromogranin A (CgA) for endocrine cells, alpha-gustducin and phospholipase C beta 2 (PLC beta 2) as taste-signaling molecules, and cystic fibrosis transmembrane regulator (CFTR) and Clara-cell-specific secretory protein of 10-kDa (CC10) as secretory markers. The results showed that amylase was present in some taste bud cells; its immunoreactivity was observed in subsets of cells that expressed CgA, alpha-gustducin, PLC beta 2, CFTR, or CC10. PGP 9.5 immunoreactivity was never colocalized with amylase. The data suggest that amylase-positive cells constitute an additional subset of taste receptor cells also associated with chemoreceptorial and/or secretory molecules, confirming the occurrence of various pathways in taste buds.

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Interaction of Saliva and Taste

Cited by 150 publications

References 62 publications

Taste function in patients with Parkinson disease

Taste function in patients with Parkinson disease

Luminal amino acid sensing in the rat gastric mucosa

Amylase expression in taste receptor cells of rat circumvallate papillae

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