Biomedical Research ; Dental Research ; Humans ; Taste ; Taste Buds ; cytology

Taste is mediated by multicellular taste buds distributed throughout the oral and pharyngeal cavities. The taste buds can detect five basic tastes: sour, sweet, bitter, salty and umami, allowing mammals to select nutritious foods and avoid the ingestion of toxic and rotten foods. Once developed, the taste buds undergo continuous renewal throughout the adult life. In the past decade, significant progress has been achived in delineating the cellular and molecular mechanisms governing taste buds development and homeostasis. With this knowledges and in-depth investigations in the future, we can achieve the precise management of taste dysfunctions such as dysgeusia and ageusia.
Animals ; Food ; Homeostasis ; Mammals ; Taste ; Taste Buds ; growth & development

Immunohistochemistry was applied to rat circumvallate papilla to localize the dopamine and norepinephrine in taste bud and to investigate the effect of preloading L-DOPA, dopamine and norepinephrine into taste cells. Dopamine and norepinephrine immunohistochemistry demonstrated that two to four taste cells except basal cells were weakly immunopositive for these neurotransmitters. Immunoreactive cells were elongated and their cell processes extended from the taste pore to the base of the taste bud. After pretreating animals with L-DOPA, four to six taste bud cells showed strong immunoreactivity for dopamine, but weak immunoreactivity for norepinephrine. Administration of dopamine or norepinephrine did not alter the number or intensity of immunoreactive cells in taste bud. These findings indicated that mammalian taste cells normally contain dopamine and norepinephrine, and that taste cells can take up L-DOPA and convert it to dopamine. Based on these findings, we postulate that norepinephrine functions as neurotransmitters or neuromodulators in taste sensory transmission.
Animals ; Dopamine ; Immunohistochemistry ; Levodopa ; Neurotransmitter Agents ; Norepinephrine ; Rats* ; Taste Buds*

OBJECTIVETo observe the ultrastructural features of taste pores and taste pits of human taste buds.

METHODSThree samplers obtained randomly from adults were divided into two perts, and transmission electron microscopy and scanning electron microscopy were used to observe the fine structure of taste buds in human circumvallate papillae.

RESULTSThe longer diameter of the taste pores was 1.02 - 7.36 microm, and most of taste pores contained no taste hair and dense material, and the profile of taste pit was triangular.

CONCLUSIONSTaste hair and dense material were seldom observed in most of taste pores.

Adult ; Humans ; Microscopy, Electron, Scanning ; Microscopy, Electron, Transmission ; Taste Buds ; ultrastructure ; Taste Perception ; Tongue ; ultrastructure

OBJECTIVES: To identify the alternative splicing isoform of mouse sweet taste receptor T1R2, and investigate the effect of lipopolysaccharide (LPS) local injection on T1R2 alternative splicing and the function of sweet taste receptor as one of the bacterial virulence factors. METHODS: After mouse taste bud tissue isolation was conducted, RNA extraction and reverse transcription polymerase chain reaction (PCR) were performed to identify the splicing isoform of T1R2. Heterologous expression experiments RESULTS: T1R2 splicing isoform T1R2_Δe3p formed sweet taste receptors with T1R3, which could not be activated by sweet taste stimuli and significantly downregulated the function of canonical T1R2/T1R3. Local LPS injection significantly increased the expression ratio of T1R2_Δe3p in mouse taste buds. CONCLUSIONS LPS stimulation affects the alternative splicing of mouse sweet taste receptor T1R2 and significantly upregulates the expression of non-functional isoform T1R2_Δe3p, suggesting that T1R2 alternative splicing regulation may be one of the mechanisms by which microbial infection affects host taste perception.
Alternative Splicing ; Animals ; Lipopolysaccharides ; Mice ; Receptors, G-Protein-Coupled/metabolism* ; Taste ; Taste Buds

The sensor of the taste is the taste bud. The signals originated from the taste buds are transmitted to the central nervous system through the gustatory taste nerves. The chorda tympani nerve (innervating the taste buds of the anterior tongue) and glossopharyngeal nerve (innervating the taste buds of the posterior tongue) are the two primary gustatory nerves. The injuries of gustatory nerves cause their innervating taste buds atrophy, degenerate and disappear. The related taste function is also impaired. The impaired taste function can be restored after the gustatory nerves regeneration. The rat model of cross-regeneration of gustatory nerves is an important platform for research in the plasticity of the central nervous system. The animal behavioral responses and the electrophysiological properties of the gustatory nerves have changed a lot after the cross-regeneration of the gustatory nerves. The effects of the injury, regeneration and cross-regeneration of the gustatory nerves on the taste function in the animals will be discussed in this review. The prospective studies on the animal model of cross-regeneration of gustatory nerves are also discussed in this review. The study on the injury, regeneration and cross-regeneration of the gustatory nerves not only benefits the understanding of mechanism for neural plasticity in gustatory nervous system, but also will provide theoretical basis and new ideas for seeking methods and techniques to cure dysgeusia.
Animals ; Chorda Tympani Nerve ; physiology ; Glossopharyngeal Nerve ; physiology ; Nerve Regeneration ; Neuronal Plasticity ; Rats ; Taste ; physiology ; Taste Buds ; physiology ; Tongue ; innervation

The dorsal lingual epithelium, which is composed of taste buds and keratinocytes differentiated from K14⁺ basal cells, discriminates taste compounds and maintains the epithelial barrier. N6-methyladenosine (m⁶A) is the most abundant mRNA modification in eukaryotic cells. How METTL3-mediated m⁶A modification regulates K14⁺ basal cell fate during dorsal lingual epithelium formation and regeneration remains unclear. Here we show knockout of Mettl3 in K14⁺ cells reduced the taste buds and enhanced keratinocytes. Deletion of Mettl3 led to increased basal cell proliferation and decreased cell division in taste buds. Conditional Mettl3 knock-in mice showed little impact on taste buds or keratinization, but displayed increased proliferation of cells around taste buds in a protective manner during post-irradiation recovery. Mechanically, we revealed that the most frequent m⁶A modifications were enriched in Hippo and Wnt signaling, and specific peaks were observed near the stop codons of Lats1 and FZD7. Our study elucidates that METTL3 is essential for taste bud formation and could promote the quantity recovery of taste bud after radiation.
Animals ; Epithelium/metabolism* ; Homeostasis ; Methylation ; Methyltransferases/metabolism* ; Mice ; RNA ; Taste Buds/metabolism*

The sweet taste receptors present in the taste buds are heterodimers comprised of T1R2 and T1R3. This receptor is also expressed in pancreatic beta-cells. When the expression of receptor subunits is determined in beta-cells by quantitative reverse transcription polymerase chain reaction, the mRNA expression level of T1R2 is extremely low compared to that of T1R3. In fact, the expression of T1R2 is undetectable at the protein level. Furthermore, knockdown of T1R2 does not affect the effect of sweet molecules, whereas knockdown of T1R3 markedly attenuates the effect of sweet molecules. Consequently, a homodimer of T1R3 functions as a receptor sensing sweet molecules in beta-cells, which we designate as sweet taste-sensing receptors (STSRs). Various sweet molecules activate STSR in beta-cells and augment insulin secretion. With regard to intracellular signals, sweet molecules act on STSRs and increase cytoplasmic Ca2+ and/or cyclic AMP (cAMP). Specifically, when an STSR is stimulated by one of four different sweet molecules (sucralose, acesulfame potassium, sodium saccharin, or glycyrrhizin), distinct signaling pathways are activated. Patterns of changes in cytoplasmic Ca2+ and/or cAMP induced by these sweet molecules are all different from each other. Hence, sweet molecules activate STSRs by acting as biased agonists.
Bias (Epidemiology)* ; Calcium ; Cyclic AMP ; Cytoplasm ; Insulin ; Polymerase Chain Reaction ; Potassium ; Reverse Transcription ; RNA, Messenger ; Saccharin ; Sodium ; Taste Buds

In rodents, the circumvallate papilla (CVP), with its underlying minor salivary gland, the von Ebners' gland (VEG), is located on the dorsal surface of the posterior tongue. Detailed morphological processes to form the proper structure of CVP and VEG have not been properly elucidated. In particular, the specific localization patterns of taste buds in CVP and the branching formation of VEG have not yet been elucidated. To understand the developmental mechanisms underlying CVP and VEG formation, detailed histological observations of CVP and VEG were examined using a three-dimensional computer-aided reconstruction method with serial histological sections and pan-Cytokeratins immunostainings. In addition, to define the developmental processes in CVP and VEG formation, we examined nerve innervations and cell proliferation using microinjections of AM1-43 and immunostainings with various markers, including phosphoinositide 3-kinase, Ki-67, PGP9.5, and Ulex europaeus agglutinin 1 (UEA1). Results revealed specific morphogenesis of CVP and VEG with nerve innervations patterns, evaluated by the coincided localization patterns of AM1-43 and UEA1. Based on these morphological and immunohistochemical results, we suggest that nerve innervations and cell proliferations play important roles in the positioning of taste buds in CVP and branching morphogenesis of VEG in tongue development.
Animals ; Cell Proliferation ; Mice ; Microinjections ; Morphogenesis ; Rodentia ; Salivary Glands, Minor ; Taste Buds ; Tongue ; Ulex ; von Ebner Glands

OBJECTIVETo observe the morphological changes and the regenerating ability of the fungiform papillae and taste buds after 60Co radiation with clinical doses in rats.

METHODSThe heads, faces and necks of 30 SD rats were radiated with a large dose and one time of 60Co in the clinical radiation. The general living condition and the number and shape of the fungiform papillae and taste buds of the tongues were observed after the radiation in rats.

RESULTSIn the group of 60Co radiation, the animals had wilting, decreasing appetite, losing weight. The heads, faces and necks of animals appeared redness, peeling of hair, increasing of secretions in 5 days after the 60Co radiation. The changes reached the summit in 10 days and the general living condition of the animals recovered in 60 days. The fungiform papillae and taste buds of the animals appeared degeneration, atrophy and collapsing in 5 days after the 60Co radiation. The injuries reached the summit in 10-20 days and the fungiform papillae and taste buds regenerated partially, and the some atrophied fungiform papillae and taste buds were not regenerated in 60 days.

CONCLUSIONThe damage to fungiform papillae and taste buds of tongue following the 60Co radiation with the clinical doses was very serious. The damaged fungiform papillae and taste buds can regenerate partially, but not completely.

Animals ; Radiation Injuries, Experimental ; pathology ; Rats ; Rats, Sprague-Dawley ; Regeneration ; Taste Buds ; pathology ; radiation effects ; Tongue ; pathology ; radiation effects