Chemical Senses最新文献

Astringency, commonly described as a drying, roughening, and/or puckering sensation associated with polyphenol-rich foods affects their palatability. While the compounds eliciting astringency are known, its mechanism of action is debated. This study investigated the role of transient receptor potential (TRP) channels A1 and V1 in astringency perception. If TRP A1 or V1 have a functional role in astringency perception, then desensitizing these receptors should decrease perceived astringency. Thirty-seven panelists underwent unilateral lingual desensitization of TRP A1 and V1 channels using mustard oil and capsaicin, respectively. Panelists then evaluated four astringent stimuli: epicatechin (EC), epigallocatechin gallate (EGCG), tannic acid (TA) and potassium alum (Alum), via 2-AFC and intensity ratings. When TRPA1 receptors were desensitized on one half of the tongue via mustard oil, no significant differences were observed between the treated and untreated sides for both 2-AFC and intensity ratings. Similarly, when TRPV1 receptors were desensitized on one half of the tongue via capsaicin, no significant differences were observed between the treated and untreated sides for both 2-AFC and intensity ratings. These findings challenge the notion that TRP channels play a pivotal role in astringency perception.

A common tool to measure olfactory function is the Sniffin' Sticks Test extended version (SSET). The SSET evaluates olfactory ability by summing the scores of three subtests: Threshold, Discrimination, and Identification. Recent meta-scientific literature revealed that many psychometric instruments currently in use have not been adequately validated, leading to a measurement crisis that raises concerns about the validity of the conclusions drawn with these instruments. Two examples of the measurement crisis are i) the use of sum scores without testing their assumptions (e.g., unidimensionality and tau-equivalence), which indicate that all subtests have the same, stable relationship with their underlying construct, and ii) the lack of assessment of measurement invariance across groups. Here, we aim to investigate the unidimensionality and tau-equivalence assumptions, internal consistency, and measurement invariance of sex and age groups of the SSET. We tested 988 (555 females, mean±SD: 39.75±18.60 years) participants with the Italian version of the SSET. The tau-equivalent model demonstrated excellent fit indices (CFI robust = 1, TLI robust = 1, RMSEA robust = 0, SRMR = .013), which best explain the data, indicating that all subtests are equally important in measuring olfactory function, but not necessarily equally precise. The results also revealed full measurement invariance across age groups and configural, partial metric, and scalar invariance across sexes, indicating that the use of latent means to compare sex groups should be chosen over raw scores. However, the SSET demonstrated moderate internal consistency. Future studies should clarify whether the reliability of the SSET can be increased.

In insects, olfactory receptor neurons (ORNs) are localized in sensilla. Within a sensillum, different ORN types are typically co-localized and exhibit non-synaptic reciprocal inhibition through ephaptic coupling. This inhibition is hypothesized to aid odour source discrimination in environments where odor molecules (odorants) are dispersed by wind, resulting in turbulent plumes. Under these conditions, odorants from a single source arrive at the ORNs synchronously, while those from separate sources arrive asynchronously. Ephaptic inhibition is expected to be weaker for asynchronous arriving odorants from separate sources, thereby enhancing their discrimination. Previous studies have focused on ephaptic inhibition of sustained ORN responses to constant odour stimuli. This begs the question of whether ephaptic inhibition also affects transient ORN responses and if this inhibition is modulated by the temporal arrival patterns of different odorants. To address this, we recorded co-localized ORNs in the fruit fly Drosophila melanogaster and exposed them to dynamic odorant mixtures. We found reciprocal inhibition, strongly suggesting the presence of ephaptic coupling. This reciprocal inhibition does indeed modulate transient ORN responses and is sensitive to the relative timing of odor stimuli. Notably, the strength of inhibition decreases as the synchrony and correlation between arriving odorants decrease. These results support the hypothesis that ephaptic inhibition aids odour source discrimination.

Terrestrial mammals identify conspecifics by body odor. Dogs can also identify humans by body odor, and in some instances, humans can identify other humans by body odor as well. Despite the potential for a powerful biometric tool, smell has not been systematically used for this purpose. A question arising in the application of smell to biometrics is which bodily odor source should we measure. Breath is an obvious candidate, but the associated humidity can challenge many sensing devices. The armpit is also a candidate source, but it is often doused in cosmetics. Here, we test the hypothesis that the ear may provide an effective source for odor-based biometrics. The inside of the ear has relatively constant humidity, cosmetics are not typically applied inside the ear, and critically, ears contain cerumen, a potent source of volatiles. We used an electronic nose to identify 12 individuals within and across days, using samples from the armpit, lower back, and ear. In an identification setting where chance was 8.33% (1 of 12), we found that we could identify a person by the smell of their ear within a day at up to ~87% accuracy (~10 of 12, binomial P < 10-5), and across days at up to ~22% accuracy (~3 of 12, binomial P < 0.012). We conclude that humans can indeed be identified from the smell of their ear, but the results did not imply a consistent advantage over other bodily odor sources.

Mammalian taste buds are highly regenerative and can restore themselves after normal wear and tear of the lingual epithelium or following physical and chemical insults, including burns, chemotherapy, and nerve injury. This is due to the continual proliferation, differentiation, and maturation of taste progenitor cells, which then must reconnect with peripheral gustatory neurons to relay taste signals to the brain. The turnover and re-establishment of peripheral taste synapses are vital to maintain this complex sensory system. Over the past several decades, the signal transduction and neurotransmitter release mechanisms within taste cells have been well delineated. However, the complex dynamics between synaptic partners in the tongue (taste cell and gustatory neuron) are only partially understood. In this review, we highlight recent findings that have improved our understanding of the mechanisms governing connectivity and signaling within the taste bud and the still-unresolved questions regarding the complex interactions between taste cells and gustatory neurons.

Taste receptor cells are morphologically classified as types II and III. Type II cells form a unique type of synapses referred to as channel synapses where calcium homeostasis modulator 1 (CALHM1) together with CALHM3 forms voltage-gated channels that release the neurotransmitter, adenosine triphosphate (ATP). To validate the proposed structural model of channel synapses, the ultrastructural localization of CALHM1 in type II cells of both fungiform and circumvallate taste buds was examined. A monoclonal antibody against CALHM1 was developed and its localization was evaluated via immunofluorescence and immunoelectron microscopy using the immunogold-silver labeling technique. CALHM1 was detected as puncta using immunofluorescence and along the presynaptic membrane of channel synapses facing atypical mitochondria, which provide ATP, by immunoelectron microscopy. In addition, it was detected along the plasma membrane lined by subsurface cisternae at sites apposed to afferent nerve fibers. Our results support the validity of a previously proposed structural model for channel synapses and provide insights into the function of subsurface cisternae whose function in taste receptor cells is unknown. We also examined the localization of CALHM1 in hybrid synapses of type III cells, which are conventional chemical synapses accompanied by mitochondria similar to atypical mitochondria of channel synapses. CALHM1 was not detected in the six hybrid synapses examined using immunoelectron microscopy. We further performed double immunolabeling for CALHM1 and Bassoon, which is detected as puncta corresponding to conventional vesicular synapses in type III cells. Our observations suggest that at least some, and probably most, hybrid synapses are not accompanied by CALHM1.