Explore the vast range of titles available.

\"A savory account of how the pursuit of delicious foods shaped human evolution\"-- Provided by publisher.

The olfactory system is exposed to external and internal harmful agents that may impair the communication between the olfactory sensory neurons and olfactory brain areas. Inflammatory molecules increase in the olfactory system in response to infections and chronic systemic diseases. Interleukin-1[beta] (IL-1[beta]) is a cytokine produced in many inflammatory processes. In previous studies, we observed that IL-1[beta] increased in the olfactory bulb (OB) of diabetic rats, which also presented olfactory dysfunction. This study aimed to determine whether IL-1[beta] could be responsible for the olfactory impairment. To address this question, IL-1[beta] and its antagonist IL-1Ra were microinjected in the OB of rats to evaluate the electrophysiological activity in the OB and entorhinal cortex (EC) by recording the local field potentials (LFPs) in resting conditions and during olfactory stimulation. RNA-seq analysis from NCBI databases demonstrated the expression of IL-1[beta] receptor 1 (IL1-R1) in the OB from rats and mice. Interestingly, IL-1[beta] reduced total spectral power in the OB and increased total signal frequency and gamma power in both OB and EC. Moreover, IL-1[beta] reduced the amplitude and increased the latency of the olfactory evoked potentials (OEPs) after OB stimulation with amyl acetate. IL-1Ra microinjection before IL-1[beta] rescued amplitude and latency of OEPs, but only partially reverted the effects of IL-1[beta] in total spectral power and relative gamma power. In addition, IL-1Ra changed the electrophysiological activity of OB and EC; however, its effect was lower than that of IL-1[beta]. These results suggest that IL-1[beta] may induce olfactory dysfunction by suppressing neuronal activity in the OB and EC. Furthermore, IL-1[beta] may also have a physiological role in the olfactory system since IL-1Ra can modify the electrical activity in these brain areas.

Animals coexist in commensal, pathogenic or mutualistic relationships with complex communities of diverse organisms, including microorganisms 1 . Some bacteria produce bioactive neurotransmitters that have previously been proposed to modulate nervous system activity and behaviours of their hosts 2 , 3 . However, the mechanistic basis of this microbiota–brain signalling and its physiological relevance are largely unknown. Here we show that in Caenorhabditis elegans , the neuromodulator tyramine produced by commensal Providencia bacteria, which colonize the gut, bypasses the requirement for host tyramine biosynthesis and manipulates a host sensory decision. Bacterially produced tyramine is probably converted to octopamine by the host tyramine β-hydroxylase enzyme. Octopamine, in turn, targets the OCTR-1 octopamine receptor on ASH nociceptive neurons to modulate an aversive olfactory response. We identify the genes that are required for tyramine biosynthesis in Providencia , and show that these genes are necessary for the modulation of host behaviour. We further find that C. elegans colonized by Providencia preferentially select these bacteria in food choice assays, and that this selection bias requires bacterially produced tyramine and host octopamine signalling. Our results demonstrate that a neurotransmitter produced by gut bacteria mimics the functions of the cognate host molecule to override host control of a sensory decision, and thereby promotes fitness of both the host and the microorganism. A neuromodulator produced by commensal Providencia bacteria that colonize the gut of Caenorhabditis elegans mimics the functions of the cognate host molecule to manipulate a sensory decision of the host.

Odours are transported in turbulent plumes, which result in rapid concentration fluctuations 1 , 2 that contain rich information about the olfactory scenery, such as the composition and location of an odour source 2 – 4 . However, it is unclear whether the mammalian olfactory system can use the underlying temporal structure to extract information about the environment. Here we show that ten-millisecond odour pulse patterns produce distinct responses in olfactory receptor neurons. In operant conditioning experiments, mice discriminated temporal correlations of rapidly fluctuating odours at frequencies of up to 40 Hz. In imaging and electrophysiological recordings, such correlation information could be readily extracted from the activity of mitral and tufted cells—the output neurons of the olfactory bulb. Furthermore, temporal correlation of odour concentrations 5 reliably predicted whether odorants emerged from the same or different sources in naturalistic environments with complex airflow. Experiments in which mice were trained on such tasks and probed using synthetic correlated stimuli at different frequencies suggest that mice can use the temporal structure of odours to extract information about space. Thus, the mammalian olfactory system has access to unexpectedly fast temporal features in odour stimuli. This endows animals with the capacity to overcome key behavioural challenges such as odour source separation 5 , figure–ground segregation 6 and odour localization 7 by extracting information about space from temporal odour dynamics. Fast temporal dynamics of the olfactory environment can be perceived by mice and used to perform scene segmentation.

Egg-laying mammals (monotremes) are the only extant mammalian outgroup to therians (marsupial and eutherian animals) and provide key insights into mammalian evolution 1 , 2 . Here we generate and analyse reference genomes of the platypus ( Ornithorhynchus anatinus ) and echidna ( Tachyglossus aculeatus ), which represent the only two extant monotreme lineages. The nearly complete platypus genome assembly has anchored almost the entire genome onto chromosomes, markedly improving the genome continuity and gene annotation. Together with our echidna sequence, the genomes of the two species allow us to detect the ancestral and lineage-specific genomic changes that shape both monotreme and mammalian evolution. We provide evidence that the monotreme sex chromosome complex originated from an ancestral chromosome ring configuration. The formation of such a unique chromosome complex may have been facilitated by the unusually extensive interactions between the multi-X and multi-Y chromosomes that are shared by the autosomal homologues in humans. Further comparative genomic analyses unravel marked differences between monotremes and therians in haptoglobin genes, lactation genes and chemosensory receptor genes for smell and taste that underlie the ecological adaptation of monotremes. New reference genomes of the two extant monotreme lineages (platypus and echidna) reveal the ancestral and lineage-specific genomic changes that shape both monotreme and mammalian evolution.

The presence of active neurogenic niches in adult humans is controversial. We focused attention to the human olfactory neuroepithelium, an extracranial site supplying input to the olfactory bulbs of the brain. Using single-cell RNA sequencing analyzing 28,726 cells, we identified neural stem cell and neural progenitor cell pools and neurons. Additionally, we detailed the expression of 140 olfactory receptors. These data from the olfactory neuroepithelium niche provide evidence that neuron production may continue for decades in humans.Durante et al. report the presence of active neurogenic niches in adult humans using single-cell RNA sequencing of the human olfactory neuroepithelium. Data from the olfactory neuroepithelium niche provide evidence that neuron production may continue for decades in humans.

Exposure to predator scents triggers an instinctive fear response in mice, including a surge in blood levels of stress hormones; here, the amygdalo-piriform transition area is identified as provoking these hormonal responses. Neural circuits responsive to predator odours Exposure to volatile predator scents triggers an instinctive fear response in mice, including a surge in the stress hormones corticotrophin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and corticosterone. Such stereotyped responses are likely to be mediated by hard-wired neural circuits, but the olfactory areas involved have so far remain unknown. Here Linda Buck and colleagues identify the amygdalo-piriform transition area as the only olfactory area upstream of hypothalamic CRH neurons that is activated by volatile predator odours, and show that this area mediates hormonal but not behavioural fear responses to these odours. Instinctive reactions to danger are critical to the perpetuation of species and are observed throughout the animal kingdom. The scent of predators induces an instinctive fear response in mice that includes behavioural changes, as well as a surge in blood stress hormones that mobilizes multiple body systems to escape impending danger 1 , 2 . How the olfactory system routes predator signals detected in the nose to achieve these effects is unknown. Here we identify a specific area of the olfactory cortex in mice that induces stress hormone responses to volatile predator odours. Using monosynaptic and polysynaptic viral tracers, we found that multiple olfactory cortical areas transmit signals to hypothalamic corticotropin-releasing hormone (CRH) neurons, which control stress hormone levels. However, only one minor cortical area, the amygdalo-piriform transition area (AmPir), contained neurons upstream of CRH neurons that were activated by volatile predator odours. Chemogenetic stimulation of AmPir activated CRH neurons and induced an increase in blood stress hormones, mimicking an instinctive fear response. Moreover, chemogenetic silencing of AmPir markedly reduced the stress hormone response to predator odours without affecting a fear behaviour. These findings suggest that AmPir, a small area comprising <5% of the olfactory cortex, plays a key part in the hormonal component of the instinctive fear response to volatile predator scents.

The omicron variant is thought to cause less olfactory dysfunction than previous variants of SARS-CoV-2, but the reported prevalence differs greatly between populations and studies. Our systematic review and meta-analysis provide information regarding regional differences in prevalence as well as an estimate of the global prevalence of olfactory dysfunction based on 62 studies reporting information on 626,035 patients infected with the omicron variant. Our estimate of the omicron-induced prevalence of olfactory dysfunction in populations of European ancestry is 11.7%, while it is significantly lower in all other populations, ranging between 1.9% and 4.9%. When ethnic differences and population sizes are considered, the global prevalence of omicron-induced olfactory dysfunction in adults is estimated to be 3.7%. Omicron’s effect on olfaction is twofold to tenfold lower than that of the alpha or delta variants according to previous meta-analyses and our analysis of studies that directly compared the prevalence of olfactory dysfunction between omicron and previous variants. The profile of the prevalence differences between ethnicities mirrors the results of a recent genome-wide association study that connected a gene locus encoding an odorant-metabolizing enzyme, UDP glycosyltransferase, to the extent of COVID-19-related loss of smell. Our analysis is consistent with the hypothesis that this enzyme contributes to the observed population differences.

Olfactory integration is important for survival in a natural habitat. However, how the nervous system processes signals of two odorants present simultaneously to generate a coherent behavioral response is poorly understood. Here, we characterize circuit basis for a form of olfactory integration in Caenorhabditis elegans . We find that the presence of a repulsive odorant, 2-nonanone, that signals threat strongly blocks the attraction of other odorants, such as isoamyl alcohol (IAA) or benzaldehyde, that signal food. Using a forward genetic screen, we found that genes known to regulate the structure and function of sensory neurons, osm-5 and osm-1 , played a critical role in the integration process. Loss of these genes mildly reduces the response to the repellent 2-nonanone and disrupts the integration effect. Restoring the function of OSM-5 in either AWB or ASH, two sensory neurons known to mediate 2-nonanone-evoked avoidance, is sufficient to rescue. Sensory neurons AWB and downstream interneurons AVA, AIB, RIM that play critical roles in olfactory sensorimotor response are able to process signals generated by 2-nonanone or IAA or the mixture of the two odorants and contribute to the integration. Thus, our results identify redundant neural circuits that regulate the robust effect of a repulsive odorant to block responses to attractive odorants and uncover the neuronal and cellular basis for this complex olfactory task.

The koala, the only extant species of the marsupial family Phascolarctidae, is classified as ‘vulnerable’ due to habitat loss and widespread disease. We sequenced the koala genome, producing a complete and contiguous marsupial reference genome, including centromeres. We reveal that the koala’s ability to detoxify eucalypt foliage may be due to expansions within a cytochrome P450 gene family, and its ability to smell, taste and moderate ingestion of plant secondary metabolites may be due to expansions in the vomeronasal and taste receptors. We characterized novel lactation proteins that protect young in the pouch and annotated immune genes important for response to chlamydial disease. Historical demography showed a substantial population crash coincident with the decline of Australian megafauna, while contemporary populations had biogeographic boundaries and increased inbreeding in populations affected by historic translocations. We identified genetically diverse populations that require habitat corridors and instituting of translocation programs to aid the koala’s survival in the wild. The assembly of the genome of the koala provides insights into its adaptive biology and identifies gene expansions that contribute to its ability to detoxify eucalyptus-derived compounds and perceive plant secondary metabolites.