Endogenous Peripheral Neuromodulators of the Mammalian Taste Bud

2010 ◽  
Vol 104 (4) ◽  
pp. 1835-1837 ◽  
Author(s):  
Robin Dando
Keyword(s):  
Taste Buds ◽  
Taste Bud ◽  
Nutritional Requirements ◽  
Short Term ◽  
Taste System ◽  
Recent Advances ◽  
The Brain ◽  
Nutritional Imbalance

The sensitivity of the mammalian taste system displays a degree of plasticity based on short-term nutritional requirements. Deficiency in a particular substance may lead to a perceived increase in palatability of this substance, providing an additional drive to redress this nutritional imbalance through modification of intake. This alteration occurs not only in the brain but also, before any higher level processing has occurred, in the taste buds themselves. A brief review of recent advances is offered.

The Sense of Taste: Neurobiology, Aging, and Medication Effects

1992 ◽  
Vol 3 (4) ◽  
pp. 371-393 ◽  
Author(s):  
Marion E. Frank ◽  
Thomas P. Hettinger ◽  
April E. Mott
Keyword(s):  
Neural Circuits ◽  
Bitter Taste ◽  
Cranial Nerves ◽  
Taste Buds ◽  
Taste Bud ◽  
Taste System ◽  
Medication Effects ◽  
Stimulus Transduction ◽  
Ventroposteromedial Nucleus ◽  
The Brain

The sense of taste is an oral chemical sense in mammals that is involved in the choice of foods. Initial transduction of taste stimuli occurs in taste buds, which are distributed in four discrete fields in the oral cavity. Medications can affect the taste buds and ion channels in taste-bud cell membranes involved in stimulus transduction. The sense of taste gradually declines with aging, with bitter taste most affected. Neural circuits that mediate taste in primates include cranial nerves VII, IX, and X, the solitary nucleus in the brain stem, the ventroposteromedial nucleus of the thalamus, and the insular-opercular cortex. The central taste pathways process taste information about sweet, salty, sour, and bitter stimuli serially and in parallel. Medications associated with "metallic" dysgeusia and taste losses affect the taste system via unknown mechanisms.

Taste Buds and Gustatory Transduction: A Functional Perspective

2021 ◽  
Author(s):  
Alan C. Spector ◽  
Susan P. Travers
Keyword(s):  
Expression Profiles ◽  
Cranial Nerves ◽  
Taste Receptor ◽  
Taste Buds ◽  
Taste Bud ◽  
Type I ◽  
Gustatory System ◽  
Type Iii ◽  
Functional Perspective ◽  
The Brain

Everything a person swallows must pass a final chemical analysis by the sensory systems of the mouth; of these, the gustatory system is cardinal. Gustation can be heuristically divided into three basic domains of function: sensory-discriminative (quality and intensity), motivational/affective (promote or deter ingestion), and physiological (e.g., salivation and insulin release). The signals from the taste buds, transmitted to the brain through the sensory branches of cranial nerves VII (facial), IX (glossopharyngeal), and X (vagal), subserve these primary functions. Taste buds are collections of 50–100 cells that are distributed in various fields in the tongue, soft palate, and throat. There are three types of cells that have been identified in taste buds based on their morphological and cytochemical expression profiles. Type II cells express specialized G-protein-coupled receptors (GPCR or GPR) on their apical membranes, which protrude through a break in the oral epithelial lining called the taste pore, that are responsible for the sensing of sweeteners (via the taste type 1 receptor (T1R) 2 + T1R3), amino acids (via the T1R1+T1R3), and bitter ligands (via the taste type 2 receptors (T2Rs)). Type III cells are critical for the sensing of acids via the otopetrin-1 (Otop-1) ion channel. The sensing of sodium, in at least rodents, occurs through the epithelial sodium channel (ENaC), but the exact composition of this channel and the type of taste cell type in which the functional version resides remains unclear. It is controversial whether Type I cells, which have been characterized as glial-like, are involved in sodium transduction or play any taste signaling role. For the most part, receptors for different stimulus classes (e.g., sugars vs. bitter ligands) are not co-expressed, providing significant early functionally related segregation of signals. There remains a persistent search for yet to be identified receptors that may contribute to some functions associated with stimuli representing the so-called basic taste qualities—sweet, salty, sour, bitter, and umami—as well as unconventional stimuli such as fatty acids (in addition to cluster of differentiation-36 (CD-36), GPR40, and GPR120) and maltodextrins. The primary neurotransmitter in taste receptor cells is ATP, which is released through a voltage-gated heteromeric channel consisting of the calcium homeostasis modulator 1 and 3 (CALHM1/3) and binds with P2X2/X3 receptors on apposed afferent fibers. Serotonin released from Type III cells has been implicated as an additional neurotransmitter, binding with HT3a receptors, and possibly playing a role in acid taste (which is sour to humans). Taste bud cells undergo complete turnover about every two weeks. Although there remains much to be understood about the operations of the taste bud, perhaps the one very clear principle that emerges is that the organization of signals transmitted to the brain is not random and arbitrary to be decoded by complex algorithms in the circuits of the central gustatory system. Rather, the transmission of taste information from the periphery is highly ordered.

scholarly journals Sprague Dawley Rats Gaining Weight on a High Energy Diet Exhibit Damage to Taste Tissue Even after Return to a Healthy Diet

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3062
Author(s):  
Fiona Harnischfeger ◽  
Flynn O’Connell ◽  
Michael Weiss ◽  
Brandon Axelrod ◽  
Andras Hajnal ◽  
...  
Keyword(s):  
High Energy ◽  
Chow Group ◽  
Taste Buds ◽  
Healthy Diet ◽  
Taste Bud ◽  
Chow Diet ◽  
Sprague Dawley ◽  
Taste System ◽  
Short Period ◽  
Taste Dysfunction

Many reports detail taste dysfunction in humans and animals with obesity. For example, mice consuming an obesogenic diet for a short period have fewer taste buds than their lean littermates. Further, rats with diet-induced obesity (DIO) show blunted electrophysiological responses to taste in the brainstem. Here, we studied the effects of high energy diet (HED)-induced peripheral taste damage in rats, and whether this deficiency could be reversed by returning to a regular chow diet. Separate groups of rats consumed a standard chow diet (Chow), a HED for 10 weeks followed by a return to chow (HED/chow), or a HED for 10 weeks followed by a restricted HED that was isocaloric with consumption by the HED/chow group (HED/isocal). Fungiform taste papilla (FP) and circumvallate taste bud abundance were quantified several months after HED groups switched diets. Results showed that both HED/chow and HED/isocal rats had significantly fewer FP and lower CV taste bud abundance than control rats fed only chow. Neutrophil infiltration into taste tissues was also quantified, but did not vary with treatment on this timeline. Finally, the number of cells undergoing programmed cell death, measured with caspase-3 staining, inversely correlated with taste bud counts, suggesting taste buds may be lost to apoptosis as a potential mechanism for the taste dysfunction observed in obesity. Collectively, these data show that DIO has lasting deleterious effects on the peripheral taste system, despite a change from a HED to a healthy diet, underscoring the idea that obesity rather than diet predicts damage to the taste system.

scholarly journals Discovery of Orgasmic Pleasure Sensing Taste Roseas of Repruductive Organs: Experimental Study

2016 ◽  
Vol 9 (1) ◽  
pp. 49-49
Author(s):  
M. Aydin ◽  
◽  
N. Aydin ◽  
C. Gundogdu ◽  
◽  
...  
Keyword(s):  
Experimental Study ◽  
Basic Mechanism ◽  
Taste Buds ◽  
Taste Bud ◽  
Glans Penis ◽  
Male Urethra ◽  
Predominant Role ◽  
Important Regulator ◽  
Computing Centers ◽  
The Brain

Objective: Basic mechanism of orgasmic pleasure hasn’t yet been elucidated, although there is broad similarity between taste and orgasmic sensation. Taste buds of tongue information has been established as important regulator of nutrition; however, very little is known regarding how orgasmic pleasure sensation is created and perceived in orgasm. Design and Method: Thus, we investigated whether there were taste bud-like structures stimulated by seminal fructose in the male urethra and glans penis. To confirm this hypothesis, we examined the urethral tissues of 22 male rabbits using the last modern histological stereological and histochemical techniques. Results: We discovered that the male urethra and glans penis contained many taste bud-like structures similar to the morphological features of the taste buds of the tongue. Interestingly, these taste bud-like structures resembling those of the tongue were detected in the intramural openings of the urethral lacunae and glandular surfaces. These structures have neuron-like appendages at the apical ends of rose buds in the wall of the urethra and glans. Moreover, each urethral plica contained some taste buds that were particularly more dense in the distal urethra, glans penis and vaginal surfaces. Conclusions: We discovered that pudendal nerves convey orgasmic sensation from the urethral taste buds to the taste information-computing centers in the brain. We postulated that urethral taste buds are stimulated by seminal fructose, and taste buds innervating nerves may play a predominant role in the creation of orgasmic sensation, which has not yet been studied so far.

scholarly journals The cell biology of taste

2010 ◽  
Vol 190 (3) ◽  
pp. 285-296 ◽  
Author(s):  
Nirupa Chaudhari ◽  
Stephen D. Roper
Keyword(s):  
Gene Expression ◽  
Cell Biology ◽  
Cellular Function ◽  
Taste Buds ◽  
Taste Bud ◽  
Cellular Organization ◽  
Current Thinking ◽  
Neuroepithelial Cells ◽  
Functional Classes ◽  
The Brain

Taste buds are aggregates of 50–100 polarized neuroepithelial cells that detect nutrients and other compounds. Combined analyses of gene expression and cellular function reveal an elegant cellular organization within the taste bud. This review discusses the functional classes of taste cells, their cell biology, and current thinking on how taste information is transmitted to the brain.

Some Observations on Changes in Denervated Taste Buds of Circumvallate Papillae of Rabbits

1969 ◽  
Vol 27 ◽  
pp. 308-309
Author(s):  
Sunao Fujimoto ◽  
Raymond G. Murray ◽  
Assia Murray
Keyword(s):  
Taste Buds ◽  
Taste Bud ◽  
Cell Type ◽  
Dark Cells ◽  
Type Iii ◽  
Circumvallate Papillae ◽  
Taste Bud Cells ◽  
Light Cells

Taste bud cells in circumvallate papillae of rabbit have been classified into three groups: dark cells; light cells; and type III cells. Unilateral section of the 9th nerve distal to the petrosal ganglion was performed in 18 animals, and changes of each cell type in the denervated buds were observed from 6 hours to 10 days after the operation.Degeneration of nerves is evident at 12 hours (Fig. 1) and by 2 days, nerves are completely lacking in the buds. Invasion by leucocytes into the buds is remarkable from 6 to 12 hours but then decreases. Their extrusion through the pore is seen. Shrinkage and disturbance in arrangement of cells in the buds can be seen at 2 days. Degenerated buds consisting of a few irregular cells and remnants of degenerated cells are present at 4 days, but buds apparently normal except for the loss of nerve elements are still present at 6 days.

Polychlorinated biphenyl induced hepatocyte alterations

1987 ◽  
Vol 45 ◽  
pp. 716-717
Author(s):  
D.N. Collins ◽  
J.N. Turner ◽  
K.O. Brosch ◽  
R.F. Seegal
Keyword(s):  
Lipid Droplets ◽  
Wistar Rats ◽  
Homovanillic Acid ◽  
Polychlorinated Biphenyl ◽  
Corn Oil ◽  
Environmental Pollutants ◽  
Short Term ◽  
Pcb Congeners ◽  
Urinary Levels ◽  
The Brain

Polychlorinated biphenyls (PCBs) are a ubiquitous class of environmental pollutants with toxic and hepatocellular effects, including accumulation of fat, proliferated smooth endoplasmic recticulum (SER), and concentric membrane arrays (CMAs) (1-3). The CMAs appear to be a membrane storage and degeneration organelle composed of a large number of concentric membrane layers usually surrounding one or more lipid droplets often with internalized membrane fragments (3). The present study documents liver alteration after a short term single dose exposure to PCBs with high chlorine content, and correlates them with reported animal weights and central nervous system (CNS) measures. In the brain PCB congeners were concentrated in particular regions (4) while catecholamine concentrations were decreased (4-6). Urinary levels of homovanillic acid a dopamine metabolite were evaluated (7).Wistar rats were gavaged with corn oil (6 controls), or with a 1:1 mixture of Aroclor 1254 and 1260 in corn oil at 500 or 1000 mg total PCB/kg (6 at each level).

Morphological Changes in the Brain of Acutely Ill and Weight-Recovered Patients with Anorexia Nervosa

2014 ◽  
Vol 42 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Cognitive Deficits ◽  
Time Course ◽  
Morphological Changes ◽  
Meta Analysis ◽  
Short Term ◽  
Clinical Prognosis ◽  
Qualitative Review ◽  
Brain Changes ◽  
The Brain

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.

scholarly journals Expression Analysis of Zinc Transporters in Nervous Tissue Cells Reveals Neuronal and Synaptic Localization of ZIP4

2021 ◽  
Vol 22 (9) ◽  
pp. 4511
Author(s):  
Chiara A. De Benedictis ◽  
Claudia Haffke ◽  
Simone Hagmeyer ◽  
Ann Katrin Sauer ◽  
Andreas M. Grabrucker
Keyword(s):  
Brain Function ◽  
Zinc Homeostasis ◽  
Zinc Transporters ◽  
Excitatory Synapses ◽  
Short Term ◽  
Synaptic Localization ◽  
Zinc Levels ◽  
Rat Astrocyte ◽  
Cellular Zinc ◽  
The Brain

In the last years, research has shown that zinc ions play an essential role in the physiology of brain function. Zinc acts as a potent neuromodulatory agent and signaling ions, regulating healthy brain development and the function of both neurons and glial cells. Therefore, the concentration of zinc within the brain and its cells is tightly controlled. Zinc transporters are key regulators of (extra-) cellular zinc levels, and deregulation of zinc homeostasis and zinc transporters has been associated with neurodegenerative and neuropsychiatric disorders. However, to date, the presence of specific family members and their subcellular localization within brain cells have not been investigated in detail. Here, we analyzed the expression of all zinc transporters (ZnTs) and Irt-like proteins (ZIPs) in the rat brain. We further used primary rat neurons and rat astrocyte cell lines to differentiate between the expression found in neurons or astrocytes or both. We identified ZIP4 expressed in astrocytes but significantly more so in neurons, a finding that has not been reported previously. In neurons, ZIP4 is localized to synapses and found in a complex with major postsynaptic scaffold proteins of excitatory synapses. Synaptic ZIP4 reacts to short-term fluctuations in local zinc levels. We conclude that ZIP4 may have a so-far undescribed functional role at excitatory postsynapses.

Adenovirus in the brain: recent advances of gene therapy for neurodegenerative diseases

1998 ◽  
Vol 55 (4) ◽  
pp. 333-341 ◽  
Author(s):  
M. Barkats ◽  
A. Bilang-Bleuel ◽  
M.H. Buc-Caron ◽  
M.N. Castel-Barthe ◽  
O. Corti ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Neurodegenerative Diseases ◽  
Recent Advances ◽  
The Brain
Sign in / Sign up

Export Citation Format

Share Document