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Biological cellular structures have inspired many scientific disciplines to design synthetic structures that can mimic their functions. Here, we closely emulate biological cellular structures in a rationally designed synthetic multicellular hybrid ion pump, composed of hydrogen-bonded [EMIM + ][TFSI − ] ion pairs on the surface of silica microstructures (artificial mechanoreceptor cells) embedded into thermoplastic polyurethane elastomeric matrix (artificial extracellular matrix), to fabricate ionic mechanoreceptor skins. Ionic mechanoreceptors engage in hydrogen bond-triggered reversible pumping of ions under external stimulus. Our ionic mechanoreceptor skin is ultrasensitive (48.1–5.77 kPa −1 ) over a wide spectrum of pressures (0–135 kPa) at an ultra-low voltage (1 mV) and demonstrates the ability to surpass pressure-sensing capabilities of various natural skin mechanoreceptors (i.e., Merkel cells, Meissner’s corpuscles, Pacinian corpuscles). We demonstrate a wearable drone microcontroller by integrating our ionic skin sensor array and flexible printed circuit board, which can control directions and speed simultaneously and selectively in aerial drone flight. Wearable pressure sensors have a range of potential applications. Here, the authors develop ion pairs decorated silica microstructures embedded in an elastomeric matrix to mimic natural skin mechanoreceptors’ functions for applications in pressure-sensitive artificial skin.

Deploying a conserved mechanosensory neuron known as the concentric hair cell, cnidarians have evolved diverse mechanoreceptors from hydroid filiform tentacles to jellyfish statocysts. However, it is unknown whether cnidarian mechanoreceptor evolution has relied solely on repurposing a single ancestral mechanosensory neuron type. Here we report evidence for cell-type diversity of mechanosensory neurons in sea-anemone cnidarian Nematostella vectensis . Uncovered in the ectoderm of feeding tentacles are conventional type I hair cells and previously unrecognized type II hair cells differing in the structure of apical sensory apparatus and synapses. Moreover, we identify TRP channel-encoding gene polycystin-1 as a type-II-hair-cell-specific essential mediator of gentle touch response. Ontogenically, type I and type II hair cells derive from distinct postmitotic precursors that begin forming at different phases of larval development. Taken together, our findings suggest that anatomically, molecularly, and developmentally distinct mechanosensory neurons diversified within Cnidaria, or prior to the divergence of Cnidaria and Bilateria. Cnidarians have evolved an array of cell types, from mechanoreceptors to stinging cells. Here they provide evidence for a diversity of mechanosensory neural cell types in a sea anemone and reveal that evolutionary histories of animal mechanosensory neurons are more complex than previously recognized.

Vincristine is an important chemotherapy drug to treat various types of cancer, but it induces peripheral neuropathy, leading to numbness and mechanical allodynia in the hands and feet of patients. The peripheral neuropathy is a dose-limiting toxicity of vincristine chemotherapy. How vincristine treatment causes numbness and mechanical allodynia remains incompletely understood. In the present study, we utilized Nav1.8-ChR2 transgenic mice in which Nav1.8-ChR2-positive and Nav1.8-ChR2-negative mechanoreceptors could be characterized using the opto-electrophysiological method. Nav1.8-ChR2-negative Aβ- and Aδ-fiber mechanoreceptors are primarily low-threshold mechanoreceptors (LTMRs). On the other hand, Nav1.8-ChR2-positive Aβ- and Aδ-fiber mechanoreceptors are mainly high-threshold mechanoreceptors (HTMRs). We have shown that the mechanical threshold of Nav1.8-ChR2-negative Aβ-fiber mechanoreceptors, but not Nav1.8-ChR2-negative Aδ-fiber mechanoreceptors, were increased significantly in the animals treated with vincristine. In contrast, the mechanical threshold of Nav1.8-ChR2-positive Aβ-fiber mechanoreceptors were significantly reduced following vincristine treatment. Vincristine treatment did not significantly affect the mechanical sensitivity of Nav1.8-ChR2-positive Aδ- and C-fiber mechanoreceptors. Vincristine treatment also did not affect the opto-sensitivity of Nav1.8-ChR2-positive Aβ-, Aδ-, and C-fiber mechanoreceptors. Our findings suggest that mechanical sensitivity is decreased in Aβ-fiber LTMRs and increased in Aβ-HTMRs following vincristine treatment, providing insights into vincristine-induced numbness and mechanical allodynia.

Sensing cooling temperatures is achieved by primary afferent endings located in the skin and is essential for the survival of animals. TRPM8 channels, primarily expressed in cutaneous C-fibers, have been established as receptors for cooling temperatures, sensing innocuous cooling from the normal skin temperature near 30°C to 17°C, and noxious cooling below 17°C. A cooling sensation is also felt when skin temperatures are first elevated to higher temperatures, for example, noxious heat, and then cool down to the normal skin temperature near 30°C. It is currently not clear what types of cutaneous afferent fibers are involved in sensing the cooling from a high heat to the normal skin temperature. Cutaneous Aβ-fiber low-threshold mechanoreceptors (Aβ-LTMRs) are primarily involved in the sense of touch and are thought to play no role in cooling sensation. In the present study, we conducted the opto-electrophysiological recordings from the skin-nerve preparations made from the hindpaw glabrous skin of Nav1.8-ChR2 transgenic mice. In these transgenic mice, Nav1.8-ChR2-negative Aβ-fiber mechanoreceptors are primarily Aβ-LTMRs, and Nav1.8-ChR2-positive Aβ-fiber mechanoreceptors are mainly high-threshold mechanoreceptors (Aβ-HTMRs). Neither Aβ-LTMRs nor Aβ-HTMRs responded to temperature rising from 30°C to the noxious heat of 43°C. However, a subpopulation of Aβ-LTMRs, but not Aβ-HTMRs, robustly fires action potential impulses in response to the temperature drop from 43°C to 30°C. This finding reveals for the first time that a subpopulation of Aβ-LTMRs senses the cooling for a temperature drop from noxious heat to normal skin temperature.

Tactile information is detected by thermoreceptors and mechanoreceptors in the skin and integrated by the central nervous system to produce the perception of somatosensation. Here we investigate the mechanism by which thermal and mechanical stimuli begin to interact and report that it is achieved by the mechanotransduction apparatus in cutaneous mechanoreceptors. We show that moderate cold potentiates the conversion of mechanical force into excitatory current in all types of mechanoreceptors from mice and tactile-specialist birds. This effect is observed at the level of mechanosensitive Piezo2 channels and can be replicated in heterologous systems using Piezo2 orthologs from different species. The cold sensitivity of Piezo2 is dependent on its blade domains, which render the channel resistant to cold-induced perturbations of the physical properties of the plasma membrane and give rise to a different mechanism of mechanical activation than that of Piezo1. Our data reveal that Piezo2 is an evolutionarily conserved mediator of thermal–tactile integration in cutaneous mechanoreceptors.

Our sense of touch emerges from an array of mechanosensory structures residing within the fabric of our skin. These tactile end organ structures convert innocuous forces acting on the skin into electrical signals that propagate to the CNS via the axons of low-threshold mechanoreceptors (LTMRs). Our rich capacity for tactile discrimination arises from the dissimilar intrinsic properties of the LTMR subtypes that innervate different regions of the skin and the structurally distinct end organ complexes with which they associate. These end organ structures comprise a range of non-neuronal cell types, which may themselves actively contribute to the transformation of tactile forces into neural impulses within the LTMR afferents. Although the mechanism and the site of transduction across end organs remain unclear, PIEZO2 has emerged as the principal mechanosensitive channel involved in light touch of the skin. Here we review the physiological properties of LTMR subtypes and discuss how features of their cutaneous end organ complexes shape subtype-specific tuning.Mammalian skin contains an array of specialized structures that transform mechanical forces into electrical signals. Handler and Ginty provide a comprehensive overview of the features of the skin’s mechanosensory end organs and the neurons with which they associate and consider how their diverse properties contribute to the sense of touch.

In mouse hairy skin, lanceolate complexes associated with three types of hair follicles, guard, awl/auchene and zigzag, serve as mechanosensory end organs. These structures are formed by unique combinations of low-threshold mechanoreceptors (LTMRs), Aβ RA-LTMRs, Aδ-LTMRs, and C-LTMRs, and their associated terminal Schwann cells (TSCs). In this study, we investigated the organization, ultrastructure, and maintenance of longitudinal lanceolate complexes at each hair follicle subtype. We found that TSC processes at hair follicles are tiled and that individual TSCs host axonal endings of more than one LTMR subtype. Electron microscopic analyses revealed unique ultrastructural features of lanceolate complexes that are proposed to underlie mechanotransduction. Moreover, Schwann cell ablation leads to loss of LTMR terminals at hair follicles while, in contrast, TSCs remain associated with hair follicles following skin denervation in adult mice and, remarkably, become re-associated with newly formed axons, indicating a TSC-dependence of lanceolate complex maintenance and regeneration in adults. Many mammals, such as cats, mice, and sea lions, have long whiskers that are particularly sensitive to touch. However, the hairs that cover the skin of most mammals are also important touch detectors. These hairs grow from follicles that are connected to the ends of the nerve cells that detect and convey touch information to the central nervous system. In mice, three main types of hair follicle—guard hairs, awl hairs, and zigzag hairs—are associated with combinations of three types of nerve endings. Much remains to be understood about how hair follicles and nerve cell endings—which are wrapped by cells called terminal Schwann cells—interact via structures called lanceolate complexes. Now, using a combination of genetics, microscopy and surgical procedures, Li and Ginty have studied these structures in unprecedented detail, and revealed some intriguing structural differences among the three types of hair follicles. Zigzag follicles—which make up the fur undercoat—are associated with fewer terminal Schwann cells than are awl follicles, whilst guard hair follicles have the most. High-resolution analyses revealed that distinct combinations of sensory nerve endings were associated with different types of hair follicle cells—which may underlie the unique responses of the different hair follicle types when the hairs are deflected. Furthermore, an individual terminal Schwann cell can be associated with more than one type of nerve ending, adding another layer of intricacy to the detection of hair movements. Killing the terminal Schwann cells in mice caused a complete loss of sensory nerve endings at hair follicles, which suggests that these cells are essential for maintaining the connection between the hair follicles and nerve cell endings. Interestingly, surgically removing nerve endings from the skin did not lead to a loss of terminal Schwann cells, and the nerve endings eventually grew back and reconnected with the hair follicles. In addition to shedding new light on the structures of lanceolate complexes in different types of hair follicles, the findings of Li and Ginty suggest that terminal Schwann cells maintain the nerve endings at hair follicles and guide their regeneration after damage. Uncovering the molecular mechanisms that control these processes represents an important next step in this research.

This study investigates the structural organization of telocytes (TCs) in the quail beak, focusing on their association with mechanoreceptors like Herbst and Ruffini corpuscles. By exploring these features, the study aim to expand the understanding of TCs’ role in mechanosensation and sensory modulation. Paraffin sections stained with Hematoxylin and Eosin revealed TCs surrounding both Herbst and Ruffini corpuscles, as well as nerve fibers. Similar findings observed using Mallory Trichrome staining, which highlighted TCs around these sensory structures. Methylene Blue staining further confirmed the presence of TCs in these areas. Semi-thin sections stained with Toluidine Blue also showed TCs encircling the sensory corpuscles, consistent with other techniques. Transmission electron microscopy (TEM) provided detailed ultrastructural insights, revealing TCs near the Herbst corpuscle, with a prominent nucleus, telopodes, and podoms, while TCs around the Ruffini corpuscle exhibited similar features. These findings have clinical relevance, as TCs increasingly recognized for their role in nerve repair and regeneration. Their involvement in sensory modulation suggests potential therapeutic applications for conditions involving nerve injury or sensory dysfunction. Immunohistochemical analysis of quail beak. Using CD34, VEGF, CD21, and CD68 IHC, TCs observed to form a three-dimensional (3D) network around the nerve. The clinical relevance of these findings was significant, as TCs increasingly recognized for their role in nerve repair and regeneration. Their involvement in sensory modulation suggests potential therapeutic avenues for conditions related to nerve injury or sensory dysfunction. Ongoing research into TCs will further deepen our understanding of their functions in sensory systems and may pave the way for novel treatments for sensory disorders.

Krause corpuscles, which were discovered in the 1850s, are specialized sensory structures found within the genitalia and other mucocutaneous tissues 1 – 4 . The physiological properties and functions of Krause corpuscles have remained unclear since their discovery. Here we report the anatomical and physiological properties of Krause corpuscles of the mouse clitoris and penis and their roles in sexual behaviour. We observed a high density of Krause corpuscles in the clitoris compared with the penis. Using mouse genetic tools, we identified two distinct somatosensory neuron subtypes that innervate Krause corpuscles of both the clitoris and penis and project to a unique sensory terminal region of the spinal cord. In vivo electrophysiology and calcium imaging experiments showed that both Krause corpuscle afferent types are A-fibre rapid-adapting low-threshold mechanoreceptors, optimally tuned to dynamic, light-touch and mechanical vibrations (40–80 Hz) applied to the clitoris or penis. Functionally, selective optogenetic activation of Krause corpuscle afferent terminals evoked penile erection in male mice and vaginal contraction in female mice, while genetic ablation of Krause corpuscles impaired intromission and ejaculation of males and reduced sexual receptivity of females. Thus, Krause corpuscles of the clitoris and penis are highly sensitive mechanical vibration detectors that mediate sexually dimorphic mating behaviours. Krause corpuscles of the clitoris and penis are highly sensitive mechanical vibration detectors that mediate sexually dimorphic mating behaviours in mice.

Collective behaviour in animal groups can improve individual perception and decision-making, but the neural mechanisms involved have been hard to access in classic models for these phenomena; here it is shown that Drosophila ’s olfactory responses are enhanced in groups of flies, through mechanosensory neuron-dependent touch interactions. How fruit-fly swarms stay in touch Schooling fish, flocking birds and human crowds can enhance the perception and decision-making of individuals in the group, but the neural mechanisms involved have been hard to determine. Richard Benton and colleagues use a more accessible model in which to study group behaviour: they show that weak odour-avoidance in individual fruitflies can be enhanced in groups of flies, thanks to cascades of appendage touch interactions between pairs of flies. By identifying the mechanosensory neurons and ion channels involved, the authors open the door to a neural-circuit dissection of collective behaviour in animal groups. Collective behaviour enhances environmental sensing and decision-making in groups of animals 1 , 2 . Experimental and theoretical investigations of schooling fish, flocking birds and human crowds have demonstrated that simple interactions between individuals can explain emergent group dynamics 3 , 4 . These findings indicate the existence of neural circuits that support distributed behaviours, but the molecular and cellular identities of relevant sensory pathways are unknown. Here we show that Drosophila melanogaster exhibits collective responses to an aversive odour: individual flies weakly avoid the stimulus, but groups show enhanced escape reactions. Using high-resolution behavioural tracking, computational simulations, genetic perturbations, neural silencing and optogenetic activation we demonstrate that this collective odour avoidance arises from cascades of appendage touch interactions between pairs of flies. Inter-fly touch sensing and collective behaviour require the activity of distal leg mechanosensory sensilla neurons and the mechanosensory channel NOMPC 5 , 6 . Remarkably, through these inter-fly encounters, wild-type flies can elicit avoidance behaviour in mutant animals that cannot sense the odour—a basic form of communication. Our data highlight the unexpected importance of social context in the sensory responses of a solitary species and open the door to a neural-circuit-level understanding of collective behaviour in animal groups.