DNA-mediated self-assembly of taste cells and neurons for taste signal transmission.

Cells can communicate with one another through physical connections and chemical signaling, activating various signaling pathways that can affect cellular functions and behaviors. In taste buds, taste cells transmit taste information to neurons via paracrine signaling. However, no previous studies have reported the in vitro co-culture of taste and neuronal cells, which allows us to monitor intercellular communications and better understand the mechanism of taste perception. Here, we introduce the first investigation on the proximate assembly and co-culture of taste cells and neurons to monitor the intercellular transmission of taste signals. Taste cells and neurons are placed closely using a pair of single-stranded oligonucleotides conjugated with polyethylene glycol and a phospholipid. Complementary oligonucleotide conjugates are anchored into the cellular membrane of neonatal taste cells and embryonic hippocampal neuronal cells, respectively, and then the cells are self-assembled into a functional multicellular unit for taste perception. Treatment of the assembled cells with a bitter tastant generates the sequential influx of calcium ions into the cytoplasm in taste cells and then in neuronal cells. Our work demonstrates that the cellular self-assembly is critical for efficient taste signal transduction, which can be used as a promising platform to construct cell-based biosensors for taste sensing.

Características dermatoscópicas de las papilas fungiformes pigmentadas de la lengua / Dermoscopic Features of Pigmented Fungiform Papillae of the Tongue

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Ryanodine receptors selectively contribute to the formation of taste-evoked calcium signals in mouse taste cells.

The peripheral taste system uses multiple signaling pathways to transduce a stimulus into an output signal that activates afferent neurons. All of these signaling pathways depend on transient increases in intracellular calcium, but current understanding of these calcium signals is not well developed. Using molecular and physiological techniques, this study establishes that ryanodine receptors (RyRs), specifically isoform 1, are expressed in taste cells and that their physiological function differs among cell types employing different signaling pathways. RyR1 contributes to some taste-evoked signals that rely on calcium release from internal stores but can also supplement the calcium signal that is initiated by opening voltage-gated calcium channels. In taste cells expressing both signaling pathways, RyR1 contributes to the depolarization-induced calcium signal but not to the calcium signal that depends on calcium release from stores. These data suggest that RyR1 is an important regulator of calcium signaling and that its physiological role in taste cells is dictated by the nature of the calcium signaling mechanisms expressed.

CD36 involvement in orosensory detection of dietary lipids, spontaneous fat preference, and digestive secretions.

Rats and mice exhibit a spontaneous attraction for lipids. Such a behavior raises the possibility that an orosensory system is responsible for the detection of dietary lipids. The fatty acid transporter CD36 appears to be a plausible candidate for this function since it has a high affinity for long-chain fatty acids (LCFAs) and is found in lingual papillae in the rat. To explore this hypothesis further, experiments were conducted in rats and in wild-type and CD36-null mice. In mice, RT-PCR experiments with primers specific for candidate lipid-binding proteins revealed that only CD36 expression was restricted to lingual papillae although absent from the palatal papillae. Immunostaining studies showed a distribution of CD36 along the apical side of circumvallate taste bud cells. CD36 gene inactivation fully abolished the preference for LCFA-enriched solutions and solid diet observed in wild-type mice. Furthermore, in rats and wild-type mice with an esophageal ligation, deposition of unsaturated LCFAs onto the tongue led to a rapid and sustained rise in flux and protein content of pancreatobiliary secretions. These findings demonstrate that CD36 is involved in oral LCFA detection and raise the possibility that an alteration in the lingual fat perception may be linked to feeding dysregulation.

Embryonic taste buds develop in the absence of innervation.

It has been hypothesized that taste buds are induced by contact with developing cranial nerve fibers late in embryonic development, since descriptive studies indicate that during embryonic development taste cell differentiation occurs concomitantly with or slightly following the advent of innervation. However, experimental evidence delineating the role of innervation in taste bud development is sparse and equivocal. Using two complementary experimental approaches, we demonstrate that taste cells differentiate fully in the complete absence of innervation. When the presumptive oropharyngeal region was taken from a donor axolotl embryo, prior to its innervation and development of taste buds, and grafted ectopically on to the trunk of a host embryo, the graft developed well-differentiated taste buds. Although grafts were invaded by branches of local spinal nerves, these neurites were rarely found near ectopic taste cells. When the oropharyngeal region was raised in culture, numerous taste buds were generated in the complete absence of neural elements. Taste buds in grafts and in explants were identical to those found in situ both in terms of their morphology and their expression of calretinin and serotonin immunoreactivity. Our findings indicate that innervation is not necessary for complete differentiation of taste receptor cells. We propose that taste buds are either induced in response to signals from other tissues, such as the neural crest, or arise independently through intrinsic patterning of the local epithelium.