Assuntos
Microcirculação , Células Receptoras Sensoriais , Pele , Humanos , Microcirculação/fisiologia , Pele/irrigação sanguínea , Pele/metabolismo , Células Receptoras Sensoriais/fisiologia , Células Receptoras Sensoriais/metabolismo , Diabetes Mellitus/metabolismo , Diabetes Mellitus/fisiopatologia , Animais , Complicações do Diabetes/fisiopatologiaRESUMO
Somatosensory neurons can sense external temperature by converting sensation of temperature information to neural activity via afferent input to the central nervous system. Various populations of somatosensory neurons have specialized gene expression, including expression of thermosensitive transient receptor potential (TRP) ion channels. Thermosensitive TRP channels are responsible for thermal transduction at the peripheral ends of somatosensory neurons and can sense a wide range of temperatures. Here we focus on several thermosensitive TRP channels including TRPV1, TRPV4, TRPM2, TRPM3, TRPM8, TRPC5, and TRPA1 in sensory neurons. TRPV3, TRPV4, and TRPC5 are also involved in somatosensation in nonneuronal cells and tissues. In particular, we discuss whether skin senses ambient temperatures through TRPV3 and TRPV4 activation in skin keratinocytes and the involvement of TRPM2 expressed by hypothalamic neurons in thermosensation in the brain.
Assuntos
Sensação Térmica , Canais de Potencial de Receptor Transitório , Humanos , Sensação Térmica/fisiologia , Sensação Térmica/genética , Animais , Canais de Potencial de Receptor Transitório/metabolismo , Canais de Potencial de Receptor Transitório/genética , Canais de Potencial de Receptor Transitório/fisiologia , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologia , Canais de Cátion TRPV/metabolismo , Canais de Cátion TRPV/genética , Pele/metabolismo , Pele/inervação , Canais de Cátion TRPM/metabolismo , Canais de Cátion TRPM/genética , Queratinócitos/metabolismoRESUMO
Temperature detection is essential for the survival and perpetuation of any species. Thermoreceptors in the skin sense the body temperature and also the temperatures of the ambient air and the objects. In 1997, Dr. David Julius and his colleagues found that a receptor expressed in small-diameter primary sensory neurons was activated by capsaicin (the pungent chemical in hot pepper). This receptor was also activated by temperature above 42 °C. That was the first time that a thermal receptor in primary sensory neurons has been identified. This receptor is named transient receptor potential vanilloid 1 (TRPV1). Now, 11 thermosensitive TRP channels are known. In this chapter, we summarize the reports and analyze thermosensitive TRP channels in a variety of ways to clarify the activation mechanisms by which temperature changes are sensed.
Assuntos
Canais de Cátion TRPV , Sensação Térmica , Canais de Potencial de Receptor Transitório , Humanos , Animais , Canais de Potencial de Receptor Transitório/metabolismo , Canais de Cátion TRPV/metabolismo , Sensação Térmica/fisiologia , Temperatura , Capsaicina/farmacologia , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologia , Termorreceptores/metabolismo , Termorreceptores/fisiologiaRESUMO
The in vivo three-dimensional genomic architecture of adult mature neurons at homeostasis and after medically relevant perturbations such as axonal injury remains elusive. Here, we address this knowledge gap by mapping the three-dimensional chromatin architecture and gene expression program at homeostasis and after sciatic nerve injury in wild-type and cohesin-deficient mouse sensory dorsal root ganglia neurons via combinatorial Hi-C, promoter-capture Hi-C, CUT&Tag for H3K27ac and RNA-seq. We find that genes involved in axonal regeneration form long-range, complex chromatin loops, and that cohesin is required for the full induction of the regenerative transcriptional program. Importantly, loss of cohesin results in disruption of chromatin architecture and severely impaired nerve regeneration. Complex enhancer-promoter loops are also enriched in the human fetal cortical plate, where the axonal growth potential is highest, and are lost in mature adult neurons. Together, these data provide an original three-dimensional chromatin map of adult sensory neurons in vivo and demonstrate a role for cohesin-dependent long-range promoter interactions in nerve regeneration.
Assuntos
Axônios , Cromatina , Coesinas , Regeneração Nervosa , Regiões Promotoras Genéticas , Células Receptoras Sensoriais , Animais , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologia , Camundongos , Regiões Promotoras Genéticas/genética , Cromatina/metabolismo , Regeneração Nervosa/genética , Regeneração Nervosa/fisiologia , Axônios/metabolismo , Axônios/fisiologia , Humanos , Proteínas Cromossômicas não Histona/metabolismo , Proteínas Cromossômicas não Histona/genética , Elementos Facilitadores Genéticos/genética , Proteínas de Ciclo Celular/metabolismo , Proteínas de Ciclo Celular/genética , Gânglios Espinais/metabolismo , Gânglios Espinais/citologia , Nervo Isquiático/metabolismoRESUMO
Temperature detection is essential for the survival and perpetuation of any species. Thermoreceptors in the skin sense body temperature as well as the temperatures of ambient air and objects. Since Dr. David Julius and his colleagues discovered that TRPV1 is expressed in small-diameter primary sensory neurons, and activated by temperatures above 42 °C, 11 of thermo-sensitive TRP channels have been identified. TRPM3 expressed in sensory neurons acts as a sensor for noxious heat. TRPM4 and TRPM5 are Ca2âº-activated monovalent cation channels, and their activity is drastically potentiated by temperature increase. This review aims to summarize the expression patterns, electrophysiological properties, and physiological roles of TRPM3, TRPM4, and TRPM5 associated with thermosensation.
Assuntos
Canais de Cátion TRPM , Canais de Cátion TRPM/metabolismo , Animais , Humanos , Sensação Térmica/fisiologia , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologia , Termorreceptores/fisiologia , Termorreceptores/metabolismoRESUMO
BACKGROUND: Sensory systems evolved intricate designs to accurately encode perplexing environments. However, this encoding task may become particularly challenging for animals harboring a small number of sensory neurons. Here, we studied how the compact resource-limited chemosensory system of Caenorhabditis elegans uniquely encodes a range of chemical stimuli. RESULTS: We find that each stimulus is encoded using a small and unique subset of neurons, where only a portion of the encoding neurons sense the stimulus directly, and the rest are recruited via inter-neuronal communication. Furthermore, while most neurons show stereotypical response dynamics, some neurons exhibit versatile dynamics that are either stimulus specific or network-activity dependent. Notably, it is the collective dynamics of all responding neurons which provides valuable information that ultimately enhances stimulus identification, particularly when required to discriminate between closely related stimuli. CONCLUSIONS: Together, these findings demonstrate how a compact and resource-limited chemosensory system can efficiently encode and discriminate a diverse range of chemical stimuli.
Assuntos
Caenorhabditis elegans , Células Quimiorreceptoras , Animais , Caenorhabditis elegans/fisiologia , Células Quimiorreceptoras/fisiologia , Células Receptoras Sensoriais/fisiologiaRESUMO
Sensory axons projecting to the central nervous system are organized into topographic maps that represent the locations of sensory stimuli. In some sensory systems, even adjacent sensory axons are arranged topographically, forming "fine-scale" topographic maps. Although several broad molecular gradients are known to instruct coarse topography, we know little about the molecular signaling that regulates fine-scale topography at the level of two adjacent axons. Here, we provide evidence that transsynaptic bone morphogenetic protein (BMP) signaling mediates local interneuronal communication to regulate fine-scale topography in the nociceptive system of Drosophila larvae. We first show that the topographic separation of the axon terminals of adjacent nociceptors requires their common postsynaptic target, the A08n neurons. This phenotype is recapitulated by knockdown of the BMP ligand, Decapentaplegic (Dpp), in these neurons. In addition, removing the Type 2 BMP receptors or their effector (Mad transcription factor) in single nociceptors impairs the fine-scale topography, suggesting the contribution of BMP signaling originated from A08n. This signaling is likely mediated by phospho-Mad in the presynaptic terminals of nociceptors to ensure local interneuronal communication. Finally, reducing Dpp levels in A08n reduces the nociceptor-A08n synaptic contacts. Our data support that transsynaptic BMP signaling establishes the fine-scale topography by facilitating the formation of topographically correct synapses. Local BMP signaling for synapse formation may be a developmental strategy that independently regulates neighboring axon terminals for fine-scale topography.
Assuntos
Proteínas Morfogenéticas Ósseas , Proteínas de Drosophila , Células Receptoras Sensoriais , Transdução de Sinais , Animais , Proteínas de Drosophila/metabolismo , Proteínas Morfogenéticas Ósseas/metabolismo , Transdução de Sinais/fisiologia , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologia , Drosophila , Larva , Nociceptores/metabolismo , Nociceptores/fisiologia , Animais Geneticamente Modificados , Sinapses/metabolismo , Sinapses/fisiologia , Terminações Pré-Sinápticas/metabolismo , Terminações Pré-Sinápticas/fisiologia , Proteínas de Ligação a DNA , Fatores de TranscriçãoRESUMO
Constructing crossmodal in-sensor processing system based on high-performance flexible devices is of great significance for the development of wearable human-machine interfaces. A bio-inspired crossmodal in-sensor computing system can perform real-time energy-efficient processing of multimodal signals, alleviating data conversion and transmission between different modules in conventional chips. Here, we report a bio-inspired crossmodal spiking sensory neuron (CSSN) based on a flexible VO2 memristor, and demonstrate a crossmodal in-sensor encoding and computing system for wearable human-machine interfaces. We demonstrate excellent performance in the VO2 memristor including endurance (>1012), uniformity (0.72% for cycle-to-cycle variations and 3.73% for device-to-device variations), speed (<30 ns), and flexibility (bendable to a curvature radius of 1 mm). A flexible hardware processing system is implemented based on the CSSN, which can directly perceive and encode pressure and temperature bimodal information into spikes, and then enables the real-time haptic-feedback for human-machine interaction. We successfully construct a crossmodal in-sensor spiking reservoir computing system via the CSSNs, which can achieve dynamic objects identification with a high accuracy of 98.1% and real-time signal feedback. This work provides a feasible approach for constructing flexible bio-inspired crossmodal in-sensor computing systems for wearable human-machine interfaces.
Assuntos
Células Receptoras Sensoriais , Dispositivos Eletrônicos Vestíveis , Humanos , Células Receptoras Sensoriais/fisiologia , Sistemas Homem-Máquina , Potenciais de Ação/fisiologia , Desenho de EquipamentoRESUMO
We developed a rat dorsal root ganglion (DRG)-derived sensory nerve organotypic model by culturing DRG explants on an organoid culture device. With this method, a large number of organotypic cultures can be produced simultaneously with high reproducibility simply by seeding DRG explants derived from rat embryos. Unlike previous DRG explant models, this organotypic model consists of a ganglion and an axon bundle with myelinated A fibers, unmyelinated C fibers, and stereo-myelin-forming nodes of Ranvier. The model also exhibits Ca2+ signaling in cell bodies in response to application of chemical stimuli to nerve terminals. Further, axonal transection increases the activating transcription factor 3 mRNA level in ganglia. Axons and myelin are shown to regenerate 14 days following transection. Our sensory organotypic model enables analysis of neuronal excitability in response to pain stimuli and tracking of morphological changes in the axon bundle over weeks.
Assuntos
Axônios , Gânglios Espinais , Sistemas Microfisiológicos , Animais , Ratos , Fator 3 Ativador da Transcrição , Axônios/fisiologia , Axônios/metabolismo , Sinalização do Cálcio , Gânglios Espinais/citologia , Gânglios Espinais/metabolismo , Bainha de Mielina/fisiologia , Bainha de Mielina/metabolismo , Organoides/metabolismo , Nervos Periféricos/metabolismo , Ratos Sprague-Dawley , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologiaRESUMO
BACKGROUND: Delivering optogenetic genes to the peripheral sensory nervous system provides an efficient approach to study and treat neurological disorders and offers the potential to reintroduce sensory feedback to prostheses users and those who have incurred other neuropathies. Adeno-associated viral (AAV) vectors are a common method of gene delivery due to efficiency of gene transfer and minimal toxicity. AAVs are capable of being designed to target specific tissues, with transduction efficacy determined through the combination of serotype and genetic promoter selection, as well as location of vector administration. The dorsal root ganglia (DRGs) are collections of cell bodies of sensory neurons which project from the periphery to the central nervous system (CNS). The anatomical make-up of DRGs make them an ideal injection location to target the somatosensory neurons in the peripheral nervous system (PNS). COMPARISON TO EXISTING METHODS: Previous studies have detailed methods of direct DRG injection in rats and dorsal horn injection in mice, however, due to the size and anatomical differences between rats and strains of mice, there is only one other published method for AAV injection into murine DRGs for transduction of peripheral sensory neurons using a different methodology. NEW METHOD/RESULTS: Here, we detail the necessary materials and methods required to inject AAVs into the L3 and L4 DRGs of mice, as well as how to harvest the sciatic nerve and L3/L4 DRGs for analysis. This methodology results in optogenetic expression in both the L3/L4 DRGs and sciatic nerve and can be adapted to inject any DRG.
Assuntos
Dependovirus , Gânglios Espinais , Técnicas de Transferência de Genes , Células Receptoras Sensoriais , Animais , Gânglios Espinais/citologia , Gânglios Espinais/metabolismo , Dependovirus/genética , Camundongos , Células Receptoras Sensoriais/fisiologia , Vetores Genéticos/administração & dosagem , Vetores Genéticos/genética , Optogenética/métodos , Masculino , Camundongos Endogâmicos C57BLRESUMO
The development of noninvasive approaches to precisely control neural activity in mammals is highly desirable. Here, we used the ion channel transient receptor potential ankyrin-repeat 1 (TRPA1) as a proof of principle, demonstrating remote near-infrared (NIR) activation of endogenous neuronal channels in mice through an engineered nanoagonist. This achievement enables specific neurostimulation in nongenetically modified mice. Initially, target-based screening identified flavins as photopharmacological agonists, allowing for the photoactivation of TRPA1 in sensory neurons upon ultraviolet A/blue light illumination. Subsequently, upconversion nanoparticles (UCNPs) were customized with an emission spectrum aligned to flavin absorption and conjugated with flavin adenine dinucleotide, creating a nanoagonist capable of NIR activation of TRPA1. Following the intrathecal injection of the nanoagonist, noninvasive NIR stimulation allows precise bidirectional control of nociception in mice through remote activation of spinal TRPA1. This study demonstrates a noninvasive NIR neurostimulation method with the potential for adaptation to various endogenous ion channels and neural processes by combining photochemical toolboxes with customized UCNPs.
Assuntos
Raios Infravermelhos , Nanopartículas , Canal de Cátion TRPA1 , Animais , Canal de Cátion TRPA1/metabolismo , Canal de Cátion TRPA1/agonistas , Camundongos , Nanopartículas/química , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologia , Células Receptoras Sensoriais/efeitos dos fármacos , Canais Iônicos/metabolismo , Nociceptividade/efeitos dos fármacosRESUMO
Dendrites of neurons receive synaptic or sensory inputs and are important sites of neuronal computation. The morphological features of dendrites not only are hallmarks of the neuronal type but also largely determine a neuron's function. Thus, dendrite morphogenesis has been a subject of intensive study in neuroscience. Quantification of dendritic morphology, which is required for accurate assessment of phenotypes, can often be a challenging task, especially for complex neurons. Because manual tracing of dendritic branches is labor-intensive and time-consuming, automated or semiautomated methods are required for efficient analysis of a large number of samples. A popular in vivo model system for studying the mechanisms of dendrite morphogenesis is dendritic arborization (da) neurons in the Drosophila larval peripheral nervous system. In this chapter, we introduce methods for visualizing and measuring the dendritic arbors of these neurons. We begin with an introduction of da neurons and an overview of the methods that have been used for measuring da neuron dendrites. We then discuss the techniques and detailed steps of neuron visualization and image acquisition. Finally, we provide example steps for dendrite tracing and measurement.
Assuntos
Dendritos , Animais , Dendritos/fisiologia , Drosophila/citologia , Larva/citologia , Células Receptoras Sensoriais/citologia , Células Receptoras Sensoriais/fisiologia , Processamento de Imagem Assistida por Computador/métodosRESUMO
Manipulation of neural circuits targeted by morphine enables pain relief without opioids.
Assuntos
Analgésicos Opioides , Morfina , Vias Neurais , Nociceptividade , Manejo da Dor , Células Receptoras Sensoriais , Animais , Humanos , Camundongos , Analgésicos Opioides/farmacologia , Morfina/farmacologia , Vias Neurais/efeitos dos fármacos , Vias Neurais/fisiologia , Nociceptividade/efeitos dos fármacos , Nociceptividade/fisiologia , Células Receptoras Sensoriais/efeitos dos fármacos , Células Receptoras Sensoriais/fisiologiaRESUMO
Epithelial damage leads to early reactive oxygen species (ROS) signaling, which regulates sensory neuron regeneration and tissue repair. How the initial type of tissue injury influences early damage signaling and regenerative growth of sensory axons remains unclear. Previously we reported that thermal injury triggers distinct early tissue responses in larval zebrafish. Here, we found that thermal but not mechanical injury impairs sensory axon regeneration and function. Real-time imaging revealed an immediate tissue response to thermal injury characterized by the rapid Arp2/3-dependent migration of keratinocytes, which was associated with tissue scale ROS production and sustained sensory axon damage. Isotonic treatment was sufficient to limit keratinocyte movement, spatially restrict ROS production, and rescue sensory neuron function. These results suggest that early keratinocyte dynamics regulate the spatial and temporal pattern of long-term signaling in the wound microenvironment during tissue repair.
Assuntos
Movimento Celular , Oxirredução , Espécies Reativas de Oxigênio , Células Receptoras Sensoriais , Transdução de Sinais , Peixe-Zebra , Animais , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologia , Espécies Reativas de Oxigênio/metabolismo , Queratinócitos/metabolismo , Queratinócitos/fisiologia , Células Epiteliais/metabolismo , Regeneração Nervosa , LarvaRESUMO
Peripheral nerve stimulation (PNS) and motor point stimulation (MPS) are noninvasive techniques used to induce muscle contraction, aiding motor function restoration in individuals with neurological disorders. Understanding sensory inputs from PNS and MPS is crucial for facilitating neuroplasticity and restoring impaired motor function. Although previous studies suggest that MPS could induce Ia-sensory inputs less than PNS, experimental evidence supporting this claim is insufficient. Here, we implemented a conditioning paradigm combining transcutaneous spinal cord stimulation (tSCS) with PNS or MPS to investigate their Ia-sensory inputs. This paradigm induces postactivation depression of spinal reflexes associated with transient decreases in neurotransmitter release from Ia-afferent terminals, allowing us to examine the Ia-sensory input amount from PNS and MPS based on the depression degree. We hypothesized that MPS would induce less postactivation depression than PNS. Thirteen individuals underwent MPS and PNS on the soleus muscle as conditioning stimuli, with tSCS applied to the skin between the spinous processes (L1-L2) as test stimuli. PNS- and MPS-conditioned spinal reflexes were recorded at five interstimulus intervals (ISIs) and four intensities. Results revealed that all PNS conditioning showed significant decreases in spinal reflex amplitudes, indicating postactivation depression. Furthermore, PNS conditioning exhibited greater depression for shorter ISIs and higher conditioning intensities. In contrast, MPS conditioning demonstrated intensity-dependent depression, but without all-conditioning depression and clear ISI dependency as seen in PNS conditioning. In addition, PNS induced significantly greater depression than MPS across most conditions. Our findings provide experimental evidence supporting the conclusion that MPS activates Ia-sensory nerves less than PNS.NEW & NOTEWORTHY Peripheral nerve stimulation (PNS) and motor point stimulation (MPS) induce neuroplasticity, but differences in their effects on Ia-sensory inputs are unclear. We investigated their Ia-sensory inputs using a conditioning paradigm with spinal reflexes. Results showed that PNS conditioning significantly inhibited spinal reflexes than MPS conditioning, indicating greater postactivation depression due to Ia-sensory nerve activation. These findings provide experimental evidence that MPS activates Ia-sensory nerves to a lesser extent than PNS, enhancing our understanding of neuroplasticity.
Assuntos
Músculo Esquelético , Humanos , Masculino , Músculo Esquelético/fisiologia , Feminino , Adulto , Estimulação Elétrica Nervosa Transcutânea/métodos , Estimulação da Medula Espinal/métodos , Adulto Jovem , Células Receptoras Sensoriais/fisiologia , Nervos Periféricos/fisiologia , Contração Muscular/fisiologiaRESUMO
Mechanosensitive ensembles of neurons in insects, known as chordotonal organs (COs), function in proprioception, the detection of sound and substrate vibrations. Here, we characterized the mechanical sensitivity of the lateral pentascolopidial CO (lch5) of Drosophila melanogaster larvae to establish its postulated role in proprioception. We developed a physiologically realistic method to replicate proprioceptive input to lch5 by pulling the apodeme (tendon) to which the tips of the neurons attach. We found that lch5 sensory neurons respond transiently with a short latency to the velocity component of stretch displacements and the release of stretch (relaxation). In the mechanosensory mutant inactive, lch5 has a decreased response to mechanical stimuli and a lower overall spontaneous spike rate. Finally, we simulated the input that lch5 receives during crawling and observed spike rate changes of peristaltic body contraction. We provide a characterization of proprioceptive feedback in D. melanogaster larvae and firmly establish the proprioceptive function of lch5 in larval locomotion.
Assuntos
Drosophila melanogaster , Larva , Propriocepção , Animais , Drosophila melanogaster/fisiologia , Larva/fisiologia , Propriocepção/fisiologia , Mecanorreceptores/fisiologia , Locomoção/fisiologia , Células Receptoras Sensoriais/fisiologia , Potenciais de Ação/fisiologia , Fenômenos BiomecânicosRESUMO
The primary sensory neurons involved in pain perception express various types of receptor-type ion channels at their nerve endings. These molecules are responsible for triggering neuronal excitation, translating environmental stimuli into pain signals. Recent studies have shown that acute nociception, induced by neuronal excitation, not only serves as a sensor for signaling life-threatening situations but also modulates our pathophysiological conditions. This modulation occurs through the release of neuropeptides by primary sensory neurons excited by nociceptive stimuli, which directly or indirectly affect peripheral systems, including immune function. Senso-immunology, an emerging research field, integrates interdisciplinary studies of pain and immunology and has garnered increasing attention in recent years. This review provides an overview of the systemic pathophysiological functions regulated by receptor-type ion channels, such as transient receptor potential (TRP) channels in primary sensory neurons, from the perspective of senso-immunology.
Assuntos
Sistema Imunitário , Células Receptoras Sensoriais , Humanos , Animais , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/imunologia , Células Receptoras Sensoriais/fisiologia , Sistema Imunitário/imunologia , Sistema Imunitário/fisiologia , Canais de Potencial de Receptor Transitório/metabolismo , Nociceptividade/fisiologia , Dor/imunologia , Dor/fisiopatologiaRESUMO
Thermosensation requires the activation of a unique collection of ion channels and receptors that work in concert to transmit thermal information. It is widely accepted that transient receptor potential melastatin 8 (TRPM8) activation is required for normal cold sensing; however, recent studies have illuminated major roles for other ion channels in this important somatic sensation. In addition to TRPM8, other TRP channels have been reported to contribute to cold transduction mechanisms in diverse sensory neuron populations, with both leak- and voltage-gated channels being identified for their role in the transmission of cold signals. Whether the same channels that contribute to physiological cold sensing also mediate noxious cold signaling remains unclear; however, recent work has found a conserved role for the kainite receptor, GluK2, in noxious cold sensing across species. Additionally, cold-sensing neurons likely engage in functional crosstalk with nociceptors to give rise to cold pain. This Review will provide an update on our understanding of the relationship between various ion channels in the transduction and transmission of cold and highlight areas where further investigation is required.
Assuntos
Temperatura Baixa , Sensação Térmica , Animais , Humanos , Sensação Térmica/fisiologia , Canais Iônicos/metabolismo , Transdução de Sinais/fisiologia , Canais de Cátion TRPM/metabolismo , Células Receptoras Sensoriais/fisiologia , Células Receptoras Sensoriais/metabolismoRESUMO
The immune and sensory nervous systems communicate to maintain homeostasis. Wu et al. recently demonstrated that sensory neurons innervate the mouse spleen. These neurons promote calcitonin gene-related peptide (CGRP)-dependent responses in splenic B cell germinal centers (GCs) and antigen-specific antibody production. Dietary capsaicin activates these neurons to enhance humoral immunity against influenza virus infection.