Oxygen electrocatalysis is of great significance in electrochemical energy conversion and storage. Many strategies have been adopted for developing advanced oxygen electrocatalysts to promote these ...technologies. In this invited contribution, recent progress in understanding the oxygen electrochemistry from theoretical and experimental aspects is summarized. The major categories of oxygen electrocatalysts, namely, noble‐metal‐based compounds, transition‐metal‐based composites, and nanocarbons, are successively discussed for oxygen reduction and evolution. Design strategies of various oxygen electrocatalysts and their relationship on the structure–activity–performance are comprehensively addressed with the perspectives. Finally, the challenge and outlook for advanced oxygen electrocatalysts are discussed toward energy conversion and storage technologies.
Design strategies of the structure‐activity‐performance relationship regarding three major categories of oxygen electrocatalysts in noble‐metal‐based, transition‐metal‐based, and carbon‐based catalysts for oxygen reduction and oxygen evolution reaction, and the corresponding oxygen electrocatalysis in three energy technologies of fuel cells, water electrolyzer, and metal‐air batteries are reviewed.
How general anesthesia (GA) induces loss of consciousness remains unclear, and whether diverse anesthetic drugs and sleep share a common neural pathway is unknown. Previous studies have revealed that ...many GA drugs inhibit neural activity through targeting GABA receptors. Here, using Fos staining, ex vivo brain slice recording, and in vivo multi-channel electrophysiology, we discovered a core ensemble of hypothalamic neurons in and near the supraoptic nucleus, consisting primarily of neuroendocrine cells, which are persistently and commonly activated by multiple classes of GA drugs. Remarkably, chemogenetic or brief optogenetic activations of these anesthesia-activated neurons (AANs) strongly promote slow-wave sleep and potentiates GA, whereas conditional ablation or inhibition of AANs led to diminished slow-wave oscillation, significant loss of sleep, and shortened durations of GA. These findings identify a common neural substrate underlying diverse GA drugs and natural sleep and reveal a crucial role of the neuroendocrine system in regulating global brain states.
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•General-anesthesia-activated neurons (AANs) are identified in hypothalamus•AANs consist mainly of neuroendocrine cells in and near the supraoptic nucleus•Activation of AANs promotes slow-wave sleep and extends general anesthesia•Inhibition of AANs shortens general anesthesia and disrupts natural sleep
Jiang-Xie et al. identified a specific group of hypothalamic neurons (AANs) commonly activated by multiple classes of general anesthetics. Stimulation of AANs potentiates slow-wave sleep and general anesthesia (GA), whereas inhibition of AANs disrupts natural sleep and destabilizes GA.
Vocalizations are fundamental to mammalian communication, but the underlying neural circuits await detailed characterization. Here, we used an intersectional genetic method to label and manipulate ...neurons in the midbrain periaqueductal gray (PAG) that are transiently active in male mice when they produce ultrasonic courtship vocalizations (USVs). Genetic silencing of PAG-USV neurons rendered males unable to produce USVs and impaired their ability to attract females. Conversely, activating PAG-USV neurons selectively triggered USV production, even in the absence of any female cues. Optogenetic stimulation combined with axonal tracing indicates that PAG-USV neurons gate downstream vocal-patterning circuits. Indeed, activating PAG neurons that innervate the nucleus retroambiguus, but not those innervating the parabrachial nucleus, elicited USVs in both male and female mice. These experiments establish that a dedicated population of PAG neurons gives rise to a descending circuit necessary and sufficient for USV production while also demonstrating the communicative salience of male USVs.
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•Specialized midbrain neurons are active when mice produce courtship vocalizations•Silencing these neurons blocks vocalization but does not impair non-vocal courtship•Activating these neurons elicits vocalization, even in the absence of social cues•Activation and tracing show that these neurons gate premotor patterning circuits
Tschida et al. use an intersectional method to identify specialized midbrain neurons whose activity is necessary and sufficient for the production of social vocalizations in the mouse, affording an entry point for genetically dissecting the brain-wide circuits for vocal communication.
General anesthesia (GA) can produce analgesia (loss of pain) independent of inducing loss of consciousness, but the underlying mechanisms remain unclear. We hypothesized that GA suppresses pain in ...part by activating supraspinal analgesic circuits. We discovered a distinct population of GABAergic neurons activated by GA in the mouse central amygdala (CeA
neurons). In vivo calcium imaging revealed that different GA drugs activate a shared ensemble of CeA
neurons. CeA
neurons also possess basal activity that mostly reflects animals' internal state rather than external stimuli. Optogenetic activation of CeA
potently suppressed both pain-elicited reflexive and self-recuperating behaviors across sensory modalities and abolished neuropathic pain-induced mechanical (hyper-)sensitivity. Conversely, inhibition of CeA
activity exacerbated pain, produced strong aversion and canceled the analgesic effect of low-dose ketamine. CeA
neurons have widespread inhibitory projections to many affective pain-processing centers. Our study points to CeA
as a potential powerful therapeutic target for alleviating chronic pain.
Humans often rank craniofacial pain as more severe than body pain. Evidence suggests that a stimulus of the same intensity induces stronger pain in the face than in the body. However, the underlying ...neural circuitry for the differential processing of facial versus bodily pain remains unknown. Interestingly, the lateral parabrachial nucleus (PB
), a critical node in the affective pain circuit, is activated more strongly by noxious stimulation of the face than of the hindpaw. Using a novel activity-dependent technology called CANE developed in our laboratory, we identified and selectively labeled noxious-stimulus-activated PB
neurons and performed comprehensive anatomical input-output mapping. Surprisingly, we uncovered a hitherto uncharacterized monosynaptic connection between cranial sensory neurons and the PB
-nociceptive neurons. Optogenetic activation of this monosynaptic craniofacial-to-PB
projection induced robust escape and avoidance behaviors and stress calls, whereas optogenetic silencing specifically reduced facial nociception. The monosynaptic circuit revealed here provides a neural substrate for heightened craniofacial affective pain.
We developed a technology (capturing activated neuronal ensembles CANE) to label, manipulate, and transsynaptically trace neural circuits that are transiently activated in behavioral contexts with ...high efficiency and temporal precision. CANE consists of a knockin mouse and engineered viruses designed to specifically infect activated neurons. Using CANE, we selectively labeled neurons that were activated by either fearful or aggressive social encounters in a hypothalamic subnucleus previously known as a locus for aggression, and discovered that social-fear and aggression neurons are intermixed but largely distinct. Optogenetic stimulation of CANE-captured social-fear neurons (SFNs) is sufficient to evoke fear-like behaviors in normal social contexts, whereas silencing SFNs resulted in reduced social avoidance. CANE-based mapping of axonal projections and presynaptic inputs to SFNs further revealed a highly distributed and recurrent neural network. CANE is a broadly applicable technology for dissecting causality and connectivity of spatially intermingled but functionally distinct ensembles.
•CANE is a new technology for capturing activated (Fos+) neuronal ensembles•CANE tags Fos+ neurons with high specificity, temporal precision, and efficiency•Hypothalamic neurons eliciting social-fear behaviors are identified using CANE•CANE-based mapping reveals a highly distributed and recurrent social-fear circuit
Sakurai et al. developed a new technology (CANE) to capture and manipulate recently activated (Fos+) neurons in the mouse brain. CANE is applied to delineate the causal functions and connectivity of hypothalamic neurons activated by a social-fear experience.
In this work, surfactant-free atomically ultrathin Rh nanosheet nanoassemblies (Rh NNs) are synthesized and used for the first time as an effective electrocatalyst in the nitrogen reduction reaction ...(NRR) at ambient temperature and pressure. The inorganic polymer RhCl 3 –K 3 Co(CN) 6 cyanogel plays an important role in the generation of ultrathin Rh nanosheets with a clean surface. Due to their unique ultrathin two-dimensional nanosheet structure ( ca. 1 nm) with a high specific surface area and modified electronic structure, the surfactant-free Rh NNs demonstrate an excellent catalytic activity for the NRR with a high production yield (NH 3 : 23.88 μg h −1 mg cat −1 ) and favorable selectivity (no N 2 H 4 generation) at low potential (−0.2 V vs. RHE), outperforming most of the current electrocatalysts reported for the NRR. Except the contribution to the efficient NRR electrocatalysis, this synthesis strategy would provide some new insights into the preparation of ultrathin precious metal nanosheets for energy related applications.
Phonation critically depends on precise controls of laryngeal muscles in coordination with ongoing respiration. However, the neural mechanisms governing these processes remain unclear. We identified ...excitatory vocalization-specific laryngeal premotor neurons located in the retroambiguus nucleus (RAm
) in adult mice as being both necessary and sufficient for driving vocal cord closure and eliciting mouse ultrasonic vocalizations (USVs). The duration of RAm
activation can determine the lengths of both USV syllables and concurrent expiration periods, with the impact of RAm
activation depending on respiration phases. RAm
neurons receive inhibition from the preBötzinger complex, and inspiration needs override RAm
-mediated vocal cord closure. Ablating inhibitory synapses in RAm
neurons compromised this inspiration gating of laryngeal adduction, resulting in discoordination of vocalization with respiration. Our study reveals the circuits for vocal production and vocal-respiratory coordination.
Pattern completion, or the ability to retrieve stable neural activity patterns from noisy or partial cues, is a fundamental feature of memory. Theoretical studies indicate that recurrently connected ...auto-associative or discrete attractor networks can perform this process. Although pattern completion and attractor dynamics have been observed in various recurrent neural circuits, the role recurrent circuitry plays in implementing these processes remains unclear. In recordings from head-fixed mice, we found that odor responses in olfactory bulb degrade under ketamine/xylazine anesthesia while responses immediately downstream, in piriform cortex, remain robust. Recurrent connections are required to stabilize cortical odor representations across states. Moreover, piriform odor representations exhibit attractor dynamics, both within and across trials, and these are also abolished when recurrent circuitry is eliminated. Here, we present converging evidence that recurrently-connected piriform populations stabilize sensory representations in response to degraded inputs, consistent with an auto-associative function for piriform cortex supported by recurrent circuitry.
Primary pain and touch sensory neurons not only detect internal and external sensory stimuli, but also receive inputs from other neurons. However, the neuronal derived inputs for primary neurons have ...not been systematically identified. Using a monosynaptic rabies viruses-based transneuronal tracing method combined with sensory-specific Cre-drivers, we found that sensory neurons receive intraganglion, intraspinal, and supraspinal inputs, the latter of which are mainly derived from the rostroventral medulla (RVM). The viral-traced central neurons were largely inhibitory but also consisted of some glutamatergic neurons in the spinal cord and serotonergic neurons in the RVM. The majority of RVM-derived descending inputs were dual GABAergic and enkephalinergic (opioidergic). These inputs projected through the dorsolateral funiculus and primarily innervated layers I, II, and V of the dorsal horn, where pain-sensory afferents terminate. Silencing or activation of the dual GABA/enkephalinergic RVM neurons in adult animals substantially increased or decreased behavioral sensitivity, respectively, to heat and mechanical stimuli. These results are consistent with the fact that both GABA and enkephalin can exert presynaptic inhibition of the sensory afferents. Taken together, this work provides a systematic view of and a set of tools for examining peri- and extrasynaptic regulations of pain-afferent transmission.
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