Browse Articles

Directing the C–N Coupling Pathway Enables Efficient Urea Electrosynthesis

Collective Biosynthesis of Plant Spirooxindole Alkaloids through Enzyme Discovery and Engineering

Direct Observation of Secondary Nucleation in Huntingtin Amyloid Formation by High-Speed Atomic Force Microscopy

A Minimalist Design for a Dual-Catalyst System for High-Efficiency Conversion of Waste Plastics into Liquid Fuel Products

Ring Expansions of 1,2-Amino Alcohols to Amine Heterocycles Enabled by Proton-Coupled Electron Transfer

Unraveling Photo-Driven H₂ Production with a Bio-Inspired NiFe Complex: Revealing an Unexpected Hydrogen Atom Source

Identification of Active Regions in a Catalyst Layer on a Gas Diffusion Electrode in the Electroreduction of CO₂

Abrupt and Gradual Changes in Neuronal Processing upon Falling Asleep and Awakening

The neural processes that change when falling asleep are only partially understood. At the cortical level, features of both spontaneous neural activity and sensory responses change between wakefulness and sleep. For example, in the early auditory cortex, sleep increases the occurrence of postonset silent (OFF) periods and elevates population synchrony. However, it remains unknown whether such changes occur abruptly or gradually around sleep onset and awakening. Here, we recorded spontaneous and sound-evoked neuronal spiking activity in the early auditory cortex along with polysomnography during thousands of episodes when male rats fell asleep or woke up. We found that when falling asleep, stimulus-induced neuronal silent periods (OFF periods), characteristic of nonrapid eye movement sleep, increased within a few seconds around sleep onset. In contrast, a gradual increase in neuronal population synchrony built up over tens of seconds until reaching maximal levels. EEG auditory-evoked potentials likely representing stimulus-triggered “K-complexes” changed along with postonset neuronal firing, whereas ongoing EEG slow-wave activity was associated with neuronal population synchrony. Similar effects, but with opposite direction, were observed around awakenings. The results highlight late stimulus-induced neuronal silence as a key feature changing abruptly around transitions between vigilance states, likely reflecting neuronal bistability and manifesting also in EEG-evoked potentials. More generally, these findings emphasize the added value of going beyond monitoring ongoing activity and perturbing the nervous system to reveal its state—an insight that could also help guide the development of more sensitive noninvasive monitors of falling asleep in humans.

Enantiocontrolled Azetidine Library Synthesis via Strain-Release Functionalization of 1-Azabicyclobutanes

Balancing *CHO/*CO Intermediate Flux via Carbonyl-Hydroxyl Motif Synergy Enables High-Selectivity Ethanol Electrosynthesis from Dilute CO_<b>2</b>

Self-Adaptive Catalysts for CO₂ Electroreduction

Sustained Hippocampal Theta Oscillations Reflect Experience-Dependent Learning in Backward Temporal Order Memory Retrieval

Navigating within our neighborhood or learning a set of concepts requires remembering the relationship between individual items that are presented sequentially. Theta activity in the mammalian hippocampus is related to the encoding and recall of relational structures. However, how theta oscillations are involved in retrieving temporal order information in opposing directionality (forward vs backward) has not been characterized. Here, using intracranial recordings from 10 human epileptic patients of both genders with hippocampal electrodes, we tested the patients with a temporal order memory task in which they learned the spatial relationship among individual items arranged along a circular track and were tested on both forward-cued and backward-cued retrieval conditions. We found that sustained high-power oscillatory events in the hippocampal theta (2–8 Hz) band, as quantified by P episode rate, were higher for the backward conditions during the later stage but not in the earlier stage. The theta P episode rate results are consistent with the behavioral memory performance and the theta phase to gamma power cross-frequency coupling. Control analyses on change in theta or gamma power and their peak frequencies, aperiodic activity, hemispheric differences, and P episode duration confirm that elevated theta rhythmic activity carry specific physiological information with respect to experience-dependent (episodic) learning. In contrast, we observed a stronger effect of forward than backward retrieval for the low gamma (30–70 Hz) P episode rate irrespective of stages. Our results revealed how theta oscillations are specifically implicated in the learning process for efficient retrieval of temporal order memories under opposing directionality.

Energy Gap Law-Harnessing Design of Highly Second Near-Infrared Emissive 34π-Annulated Porphyrinoids for In Vivo Imaging

The Epigenetic Reader PHF23 Is Required for Embryonic Neurogenesis

Epigenetic mechanisms are crucial in the tightly regulated process of neurogenesis from radial glial cells (RGCs) to intermediate progenitor cells (IPCs) to neurons during embryonic brain development. Plant homeodomain (PHD) finger proteins as important epigenetic readers are implicated in development and diseases, yet their roles in embryonic neurogenesis remain largely unexplored. In this study, we found different PHD finger proteins are differentially expressed along the neurogenesis trajectory. Among them, we investigated the function of PHF23 using mouse models, which is highly expressed in RGCs and IPCs, but not in neurons. Our findings demonstrate that PHF23 is essential for proper neurogenesis, and Phf23 knock-out ( Phf2 3-KO) results in cortical developmental defects due to differentiation blockade of RGCs. Mechanistically, PHF23 bind with HDAC2, inhibiting its deacetylation activity on the active histone mark H3K27ac, thereby promoting the expression of neuronal differentiation pathway genes such as Tcf4 and Eya1 . Overexpression of Tcf4 rescues the differentiation defects of Phf2 3-KO NSCs. These results establish PHF23 as a pivotal regulator of neurogenesis, indicating cell type-specific functions of PHD finger proteins.

Silicon: A Surface Dopant for Stable Alumina-Supported PtGa Propane Dehydrogenation Catalysts by Favoring Redox and Carbon Dynamics

Benchmarking the Reactivity of Caged Iron(IV)-Oxo Sites within Metal–Organic Frameworks

Electrokinetic Detection of Single-Molecule Phosphorylation

Distinct Regulation of Early Trafficking of the NMDA Receptors by the Ligand-Binding Domains of the GluN1 and GluN2A Subunits

N -Methyl- d -aspartate receptors (NMDARs) play a crucial role in excitatory neurotransmission, with numerous pathogenic variants identified in the GluN subunits, including their ligand-binding domains (LBDs). The prevailing hypothesis postulates that the endoplasmic reticulum (ER) quality control machinery verifies the agonist occupancy of NMDARs, but this was tested in a limited number of studies. Using microscopy and electrophysiology in the human embryonic kidney 293 (HEK293) cells, we found that surface expression of GluN1/GluN2A receptors containing a set of alanine substitutions within the LBDs correlated with the measured EC 50 values for glycine (GluN1 subunit mutations) while not correlating with the measured EC 50 values for l -glutamate (GluN2A subunit mutations). The mutant cycle of GluN1-S688 residue, including the pathogenic GluN1-S688Y and GluN1-S688P variants, showed a correlation between relative surface expression of the GluN1/GluN2A receptors and the measured EC 50 values for glycine, as well as with the calculated Δ G binding values for glycine obtained from molecular dynamics simulations. In contrast, the mutant cycle of GluN2A-S511 residue did not show any correlation between the relative surface expression of the GluN1/GluN2A receptors and the measured EC 50 values for l -glutamate or calculated Δ G binding values for l -glutamate. Coexpression of both mutated GluN1 and GluN2A subunits led to additive or synergistic alterations in the surface number of GluN1/GluN2A receptors. The synchronized ER release by ARIAD technology confirmed the altered early trafficking of GluN1/GluN2A receptors containing the mutated LBDs. The microscopical analysis from embryonal rat hippocampal neurons (both sexes) corroborated our conclusions from the HEK293 cells.

Tuning the Supramolecular Polymerization and Cell Response of Ureidopyrimidinone Monomers by Pushing the Hydrophobic Threshold

High-Connected Ternary Metal–Organic Framework Platform: Synthesis, Structure, and Methane Storage Capacity