scholarly journals Integrating TRPV1 Receptor Function with Capsaicin Psychophysics

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Gregory Smutzer ◽  
Roni K. Devassy

Capsaicin is a naturally occurring vanilloid that causes a hot, pungent sensation in the human oral cavity. This trigeminal stimulus activates TRPV1 receptors and stimulates an influx of cations into sensory cells. TRPV1 receptors function as homotetramers that also respond to heat, proinflammatory substances, lipoxygenase products, resiniferatoxin, endocannabinoids, protons, and peptide toxins. Kinase-mediated phosphorylation of TRPV1 leads to increased sensitivity to both chemical and thermal stimuli. In contrast, desensitization occurs via a calcium-dependent mechanism that results in receptor dephosphorylation. Human psychophysical studies have shown that capsaicin is detected at nanomole amounts and causes desensitization in the oral cavity. Psychophysical studies further indicate that desensitization can be temporarily reversed in the oral cavity if stimulation with capsaicin is resumed at short interstimulus intervals. Pretreatment of lingual epithelium with capsaicin modulates the perception of several primary taste qualities. Also, sweet taste stimuli may decrease the intensity of capsaicin perception in the oral cavity. In addition, capsaicin perception and hedonic responses may be modified by diet. Psychophysical studies with capsaicin are consistent with recent findings that have identified TRPV1 channel modulation by phosphorylation and interactions with membrane inositol phospholipids. Future studies will further clarify the importance of capsaicin and its receptor in human health and nutrition.

2011 ◽  
Vol 56 (No. 12) ◽  
pp. 612-618 ◽  
Author(s):  
P. Cizek ◽  
L. Krejcirova ◽  
I. Kocianova ◽  
F. Tichy

Reptiles have recently become a popular group of pet animals. A relatively large number of studies on the morphology of the oral cavity and method of feeding in adult individuals have been published. Nevertheless, embryological descriptions of reptile body parts or structures are rare. In this study, we describe the morphology of the developing tongue, in particular its dorsal surface, in pre-hatched green iguanas. Microscopic examination of the oral cavity of early embryos revealed that the tongue was divided into three different areas: apex, corpus and radix. The dorsal lingual surface was smooth and covered by nonkeratinised stratified squamous epithelium with slight prominences in some cases. In the underlying mesenchyme of the tongue, striated muscular tissue was formed. The epithelium thickness was reduced during formation of the lingual papillae and in later stages remained simple cuboidal. No developing taste buds could be recognised in the lingual epithelium.  


2002 ◽  
Vol 22 (7) ◽  
pp. 2194-2203 ◽  
Author(s):  
Alexander Pulvermüller ◽  
Andreas Gießl ◽  
Martin Heck ◽  
Ralf Wottrich ◽  
Angelika Schmitt ◽  
...  

ABSTRACT Photoexcitation of rhodopsin activates a heterotrimeric G-protein cascade leading to cyclic GMP hydrolysis in vertebrate photoreceptors. Light-induced exchanges of the visual G-protein transducin between the outer and inner segment of rod photoreceptors occur through the narrow connecting cilium. Here we demonstrate that transducin colocalizes with the Ca2+-binding protein centrin 1 in a specific domain of this cilium. Coimmunoprecipitation, centrifugation, centrin overlay, size exclusion chromatography, and kinetic light-scattering experiments indicate that Ca2+-activated centrin 1 binds with high affinity and specificity to transducin. The assembly of centrin-G-protein complex is mediated by the βγ-complex. The Ca2+-dependent assembly of a G protein with centrin is a novel aspect of the supply of signaling proteins in sensory cells and a potential link between molecular translocations and signal transduction in general.


2021 ◽  
Author(s):  
Anoumid Vaziri ◽  
Daniel Wilinski ◽  
Peter Freddolino ◽  
Carrie Ferrario ◽  
MONICA DUS

Diet composition has a profound influence on brain physiology and behavior, but the mechanisms through which nutrient information is transmuted into neural changes remain elusive. Here we uncover how the metabolic enzyme O-GlcNAc Transferase (OGT) transforms information about the dietary environment into taste adaptations. We show that in the fly D. melanogaster, OGT decorates the chromatin of the sweet taste neurons and provides the nutrient context to drive changes in chromatin accessibility in response to high dietary sugar. Specifically, we found that OGT cooperates with the epigenetic silencer Polycomb Repressive Complex 2.1 (PRC2.1) to promote nutrient-sensitive variations in chromatin openness; these chromatin dynamics result in changes in gene expression and taste plasticity that are dependent on the catalytic activity of OGT. Parallel nutrigenomic signatures were also observed in the lingual epithelium of rats exposed to high dietary sugar, suggesting that this conserved metabolic-epigenetic pathway may also underlie diet-dependent taste changes in mammals. Together our findings reveal a novel role for nutriepigenetic signaling in the brain: amplifying nutrient perturbations into robust changes in chromatin accessibility and transcriptional output that shape neural and behavioral plasticity.


2015 ◽  
Vol 308 (1) ◽  
pp. C21-C32 ◽  
Author(s):  
Robin Dando ◽  
Elizabeth Pereira ◽  
Mani Kurian ◽  
Rene Barro-Soria ◽  
Nirupa Chaudhari ◽  
...  

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.


2008 ◽  
Vol 295 (1) ◽  
pp. L201-L213 ◽  
Author(s):  
Anne-Christine Peyter ◽  
Vincent Muehlethaler ◽  
Lucas Liaudet ◽  
Mathieu Marino ◽  
Stefano Di Bernardo ◽  
...  

Perinatal adverse events such as limitation of nutrients or oxygen supply are associated with the occurrence of diseases in adulthood, like cardiovascular diseases and diabetes. We investigated the long-term effects of perinatal hypoxia on the lung circulation, with particular attention to the nitric oxide (NO)/cGMP pathway. Mice were placed under hypoxia in utero 5 days before delivery and for 5 days after birth. Pups were then bred in normoxia until adulthood. Adults born in hypoxia displayed an altered regulation of pulmonary vascular tone with higher right ventricular pressure in normoxia and increased sensitivity to acute hypoxia compared with controls. Perinatal hypoxia dramatically decreased endothelium-dependent relaxation induced by ACh in adult pulmonary arteries (PAs) but did not influence NO-mediated endothelium-independent relaxation. The M3 muscarinic receptor was implicated in the relaxing action of ACh and M1 muscarinic receptor (M1AChR) in its vasoconstrictive effects. Pirenzepine or telenzepine, two preferential inhibitors of M1AChR, abolished the adverse effects of perinatal hypoxia on ACh-induced relaxation. M1AChR mRNA expression was increased in lungs and PAs of mice born in hypoxia. The phosphodiesterase 1 (PDE1) inhibitor vinpocetine also reversed the decrease in ACh-induced relaxation following perinatal hypoxia, suggesting that M1AChR-mediated alteration of ACh-induced relaxation is due to the activation of calcium-dependent PDE1. Therefore, perinatal hypoxia leads to an altered pulmonary circulation in adulthood with vascular dysfunction characterized by impaired endothelium-dependent relaxation and M1AChR plays a predominant role. This raises the possibility that muscarinic receptors could be key determinants in pulmonary vascular diseases in relation to “perinatal imprinting.”


2002 ◽  
Vol 80 (10) ◽  
pp. 1772-1794 ◽  
Author(s):  
G Kass-Simon ◽  
A A Scappaticci, Jr.

Nematocysts are the nonliving secretions of specialized cells, the nematocytes, which develop from multipotent stem cells. Nematocysts are the means by which coelenterates capture prey and defend against predation. The 25 or more known types of nematocysts can be divided into to four functional categories: those that pierce, ensnare, or adhere to prey, and those that adhere to the substrate. During development a collagenous cyst, which may contain toxins, forms; a hollow thread, which becomes coiled as it invaginates, develops. Maturing nematocyte–nematocyst complexes migrate to their discharge sites and are deployed in specific patterns. The mechanisms of pattern determination are not clear. Discharge of nematocysts appears to involve increases in intracapsular osmotic pressure consequent upon release of bound calcium within the capsule; the eversion of the filament may depend upon release of structural tension consequent upon a loss of zinc from the thread. Evidence exists that discharge is initiated as a calcium-dependent exocytosis, triggered by an electrical signal resulting from the transduction of mechanical stimuli received at the nematocyte's cnidocil. Chemical signals transduced in adjacent sensory cells alter the frequency response of the nematocyte. In opposition to the nematocyte–nematocyst independent effector hypothesis, excitatory and inhibitory neuronal input appears to regulate discharge.


2021 ◽  
Vol 46 ◽  
Author(s):  
Satoshi Fukuda ◽  
Naoyuki Murabe ◽  
Haruno Mizuta ◽  
Takashi Yamamoto ◽  
Takatoshi Nagai

Abstract The lingual surface potential (LSP), which hyperpolarizes in response to salt and bitter stimuli, is thought to be a bioelectrical signal associated with taste transduction in humans. In contrast, a recent study reported sweet and sour stimuli to evoke a depolarization of the LSP. We questioned the origin of such a depolarization because liquid junction potentials (JPs), which arise at the interfaces of recording electrode and taste solutions, are neglected in the report. We recorded the LSPs to sucrose and NaCl solutions on the human tongue using an Ag/AgCl electrode. To estimate JPs generated by each taste solution, we made an agar model to simulate the human tongue. The lingual surface was rinsed with a 10 mM NaCl solution that mimics the sodium content of the lingual fluid. In the human tongue, sucrose dissolved in distilled water evoked a depolarizing LSP that could be attributed to JPs, resulting from the change in electrolyte concentration of the taste solution. Sucrose dissolved in 10 mM NaCl solution evoked a hyperpolarizing LSP which became more negative in a concentration-dependent manner (300–1500 mM). Lactisole (3.75 mM), an inhibitor of sweet taste, significantly reduced the LSPs and decreased perceived intensity of sweetness by human subjects. The negative JPs generated by 100 mM NaCl in the agar model were not different from the LSPs to 100 mM NaCl. When the electrolyte environment on the lingual surface is controlled for JPs, the bioelectrical signal associated with sweet taste transduction is a hyperpolarizing potential.


1998 ◽  
Vol 274 (1) ◽  
pp. C182-C191 ◽  
Author(s):  
Ingrid Jakob ◽  
Ingeborg A. Hauser ◽  
Frank Thévenod ◽  
Bernd Lindemann

Multidrug resistance P-glycoprotein (MDR1) is a membrane protein of 150–170 kDa that catalyzes the ATP-driven efflux of hydrophobic xenobiotics, including fluorescent dyes, from cells. Expressed in many epithelial tissues and in the endothelia of the blood-brain barrier, the MDR1 protein provides major routes of detoxification. We found that taste cells of the rat vallate papilla (VP; posterior tongue) had only a slow increase in fluorescence due to uptake of the hydrophobic dye calcein acetoxymethyl ester. However, the development of fluorescence was accelerated two- to threefold by substrates and/or inhibitors of MDR1, such as verapamil, tamoxifen, and cyclosporin A, and by addition of the transport-blocking antibody to MDR1, UIC2. Western blots of vallate tissue rich in taste buds with the MDR1-specific monoclonal antibodies C219 and C494 revealed an immunoreactive protein at ∼170 kDa. In contrast, the lingual epithelium surrounding the VP showed a much weaker band with these antibodies. Furthermore, using the antibodies C494 and UIC2 with tissue sections, MDR1-like immunoreactivity was found in taste cells. These results show that MDR1 is present and functional in vallate taste cells of the rat. MDR1-related transport may achieve active elimination of xenobiotics from the sensory cells and thereby protect the peripheral taste organs from potentially harmful molecules contained in an animal’s food.


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