Explore the vast range of titles available.

The human olfactory system comprises olfactory receptor neurons, projection neurons, and interneurons that perform remarkably sophisticated functions, including sensing, filtration, memorization, and forgetting of chemical stimuli for perception. Developing an artificial olfactory system that can mimic these functions has proved to be challenging. Herein, inspired by the neuronal network inside the glomerulus of the olfactory bulb, we present an artificial chemosensory neuronal synapse that can sense chemical stimuli and mimic the functions of excitatory and inhibitory neurotransmitter release in the synapses between olfactory receptor neurons, projection neurons, and interneurons. The proposed device is based on a flexible organic electrochemical transistor gated by the potential generated by the interaction of gas molecules with ions in a chemoreceptive ionogel. The combined use of a chemoreceptive ionogel and an organic semiconductor channel allows for a long retentive memory in response to chemical stimuli. Long-term memorization of the excitatory chemical stimulus can be also erased by applying an inhibitory electrical stimulus due to ion dynamics in the chemoresponsive ionogel gate electrolyte. Applying a simple device design, we were able to mimic the excitatory and inhibitory synaptic functions of chemical synapses in the olfactory system, which can further advance the development of artificial neuronal systems for biomimetic chemosensory applications. Developing an artificial olfactory system that can mimic the biological functions remains a challenge. Here, the authors develop an artificial chemosensory synapse based on a flexible organic electrochemical transistor gated by the potential generated by the interaction of gas molecules with ions in a chemoreceptive ionogel.

Mosquitoes are important vectors of disease and require sources of carbohydrates for reproduction and survival. Unlike host-related behaviors of mosquitoes, comparatively less is understood about the mechanisms involved in nectar-feeding decisions, or how this sensory information is processed in the mosquito brain. Here we show that Aedes spp. mosquitoes, including Aedes aegypti, are effective pollinators of the Platanthera obtusata orchid, and demonstrate this mutualism is mediated by the orchid’s scent and the balance of excitation and inhibition in the mosquito’s antennal lobe (AL). The P. obtusata orchid emits an attractive, nonanal-rich scent, whereas related Platanthera species—not visited by mosquitoes—emit scents dominated by lilac aldehyde. Calcium imaging experiments in the mosquito AL revealed that nonanal and lilac aldehyde each respectively activate the LC2 and AM2 glomerulus, and remarkably, the AM2 glomerulus is also sensitive to N,N-diethylmeta-toluamide (DEET), a mosquito repellent. Lateral inhibition between these 2 glomeruli reflects the level of attraction to the orchid scents. Whereas the enriched nonanal scent of P. obtusata activates the LC2 and suppresses AM2, the high level of lilac aldehyde in the other orchid scents inverts this pattern of glomerular activity, and behavioral attraction is lost. These results demonstrate the ecological importance of mosquitoes beyond operating as disease vectors and open the door toward understanding the neural basis of mosquito nectar-seeking behaviors.

Olfactory neurons respond to various odorants according to which olfactory receptors, of many, they express. During development, axons from olfactory neurons that express the same olfactory receptor converge to share the same glomeruli. Nakashima et al. now show that, in mice, the neurons build these connections according to shared patterns of activity. When the olfactory receptor is triggered, it causes its cell not simply to fire but to fire in specific patterns. Neurons that speak the same code end up connected at the same glomerulus. Science , this issue p. eaaw5030 The temporal pattern of neuronal firing rather than its synchronicity refines olfactory codes in the brain. Neural circuits emerge through the interplay of genetic programming and activity-dependent processes. During the development of the mouse olfactory map, axons segregate into distinct glomeruli in an olfactory receptor (OR)–dependent manner. ORs generate a combinatorial code of axon-sorting molecules whose expression is regulated by neural activity. However, it remains unclear how neural activity induces OR-specific expression patterns of axon-sorting molecules. We found that the temporal patterns of spontaneous neuronal spikes were not spatially organized but were correlated with the OR types. Receptor substitution experiments demonstrated that ORs determine spontaneous activity patterns. Moreover, optogenetically differentiated patterns of neuronal activity induced specific expression of the corresponding axon-sorting molecules and regulated axonal segregation. Thus, OR-dependent temporal patterns of spontaneous activity play instructive roles in generating the combinatorial code of axon-sorting molecules during olfactory map formation.

The vertebrate clustered protocadherin (Pcdh) cell surface proteins are encoded by three closely linked gene clusters (Pcdhα, Pcdhβ, and Pcdhγ). Here, we show that all three gene clusters functionally cooperate to provide individual mouse olfactory sensory neurons (OSNs) with the cell surface diversity required for their assembly into distinct glomeruli in the olfactory bulb. Although deletion of individual Pcdh clusters had subtle phenotypic consequences, the loss of all three clusters (tricluster deletion) led to a severe axonal arborization defect and loss of self-avoidance. By contrast, when endogenous Pcdh diversity is overridden by the expression of a single–tricluster gene repertoire (α and β and γ), OSN axons fail to converge to form glomeruli, likely owing to contact-mediated repulsion between axons expressing identical combinations of Pcdh isoforms.

A globally invasive form of the mosquito Aedes aegypti specializes in biting humans, making it an efficient disease vector 1 . Host-seeking female mosquitoes strongly prefer human odour over the odour of animals 2 , 3 , but exactly how they distinguish between the two is not known. Vertebrate odours are complex blends of volatile chemicals with many shared components 4 – 7 , making discrimination an interesting sensory coding challenge. Here we show that human and animal odours evoke activity in distinct combinations of olfactory glomeruli within the Ae. aegypti antennal lobe. One glomerulus in particular is strongly activated by human odour but responds weakly, or not at all, to animal odour. This human-sensitive glomerulus is selectively tuned to the long-chain aldehydes decanal and undecanal, which we show are consistently enriched in human odour and which probably originate from unique human skin lipids. Using synthetic blends, we further demonstrate that signalling in the human-sensitive glomerulus significantly enhances long-range host-seeking behaviour in a wind tunnel, recapitulating preference for human over animal odours. Our research suggests that animal brains may distil complex odour stimuli of innate biological relevance into simple neural codes and reveals targets for the design of next-generation mosquito-control strategies. Select chemical compounds enriched in human odour activate an olfactory glomerulus in the brain of Aedes aegypti mosquitoes, which strengthens host-seeking behaviour and helps explain their strong preference for biting humans.

Memory is coded by patterns of neural activity in distinct circuits. Therefore, it should be possible to reverse engineer a memory by artificially creating these patterns of activity in the absence of a sensory experience. In olfactory conditioning, an odor conditioned stimulus (CS) is paired with an unconditioned stimulus (US; for example, a footshock), and the resulting CS–US association guides future behavior. Here we replaced the odor CS with optogenetic stimulation of a specific olfactory glomerulus and the US with optogenetic stimulation of distinct inputs into the ventral tegmental area that mediate either aversion or reward. In doing so, we created a fully artificial memory in mice. Similarly to a natural memory, this artificial memory depended on CS–US contingency during training, and the conditioned response was specific to the CS and reflected the US valence. Moreover, both real and implanted memories engaged overlapping brain circuits and depended on basolateral amygdala activity for expression.Pairing an odor conditioned stimulus (CS) with an unconditioned stimulus (US) induces memory formation. Vetere et al. replace the real CS and US with direct optogenetic stimulation of the brain and create a fully artificial odor memory in mice.

Discriminative learning enhances contrast between sensory inputs to allow fast and accurate decision-making. However, the neural mechanisms that selectively enhance sensory representations to improve discrimination remain unclear. Here, we show that learning-induced differential gating of olfactory inputs takes place at the first stage of sensory processing in the mouse olfactory bulb and requires dopaminergic short axons cells (SACs). Optical imaging, spatial transcriptomics, and electron microscopy experiments reveal that synaptic and structural plasticity in SACs allows odor valence-based modulation of their interactions with other cell types in the olfactory glomeruli. Importantly, an increase in tyrosine hydroxylase expression by SACs surrounding responding glomeruli, with a bias towards those activated by reward odors, creates a valence-based modulation of sensory input. Further, we identify cholinergic input from the horizontal limb of the diagonal band as the valence-dependent signal that modulates SAC activities and refines sensory representation via disinhibition. Our findings reveal a circuit mechanism where an interneuron population serves as a central hub integrating sensory input and top–down signal to enhance sensory acuity.

Inputs from olfactory sensory neuron (OSN) axons expressing the same type of odorant receptor (OR) converge in the glomerulus of the main olfactory bulb. A key marker of mature OSNs is olfactory marker protein (OMP), whose deletion has been associated with deficits in OSN signal transduction and odor discrimination. Here, we investigate glomerular odor responses and anatomical architecture in mice in which one or both alleles of OMP are replaced by the fluorescent synaptic activity reporter, synaptopHluorin. Functionally heterogeneous glomeruli, that is, ones with microdomains with distinct odor responses, are rare in OMP +/– mice, but occur frequently in OMP –/– mice. Genetic targeting of single ORs reveals that these microdomains arise from co-innervation of individual glomeruli by OSNs expressing different ORs. This glomerular mistargeting is locally restricted to a few glomerular diameters. Our studies document functional heterogeneity in sensory input within individual glomeruli and uncover its anatomical correlate, revealing an unexpected role for OMP in the formation and refinement of the glomerular map. Olfactory marker protein (OMP) expressed in all olfactory sensory neurons (OSN) is required for proper signal transduction and odor discrimination. Here, the authors report that OMP deletion leads to formation of glomeruli with axons from heterogeneous OSNs due to local axonal mistargeting.

Evaluating odor blends in sensory processing is a crucial step for signal recognition and execution of behavioral decisions. Using behavioral assays and 2-photon imaging, we have characterized the neural and behavioral correlates of mixture perception in the olfactory system of Drosophila . Mixtures of odors with opposing valences elicit strong inhibition in certain attractant-responsive input channels. This inhibition correlates with reduced behavioral attraction. We demonstrate that defined subsets of GABAergic interneurons provide the neuronal substrate of this computation at pre- and postsynaptic loci via GABA B - and GABA A receptors, respectively. Intriguingly, manipulation of single input channels by silencing and optogenetic activation unveils a glomerulus-specific crosstalk between the attractant- and repellent-responsive circuits. This inhibitory interaction biases the behavioral output. Such a form of selective lateral inhibition represents a crucial neuronal mechanism in the processing of conflicting sensory information. Fruit flies need to appropriately respond to mixtures of attractive and repellent odors in their natural environment. Here, the authors propose that lateral inhibition between glomeruli activated by attractants or repulsive odors mediates the appropriate response.

Odorants stimulate olfactory sensory neurons (OSNs) to create a bilateral sensory map defined by a set of glomeruli present in the left and right olfactory bulbs. Using Xenopus tropicalis tadpoles, we challenged the notion that glomerular activation is exclusively determined ipsilaterally. Glomerular responses evoked by unilateral stimulation were potentiated following transection of the contralateral olfactory nerve. The gain of function was observed as early as 2 hr after injury and faded away with a time constant of 4 days. Potentiation was mediated by the presence of larger and faster calcium transients driving glutamate release from OSN axon terminals. The cause was the reduction of the tonic presynaptic inhibition exerted by dopamine D 2 receptors. Inflammatory mediators generated by injury were not involved. These findings reveal the presence of a bilateral modulation of glomerular output driven by dopamine that compensates for imbalances in the number of operative OSNs present in the two olfactory epithelia. Considering that the constant turnover of OSNs is an evolutionarily conserved feature of the olfactory system and determines the innervation of glomeruli, the compensatory mechanism described here may represent a general property of the vertebrate olfactory system to establish an odor map.