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Correction to “Stacking Faults Assist Lithium-Ion Conduction in a Halide-Based Superionic Conductor”

Prioritizing Working Memory Resources Depends on the Prefrontal Cortex

How the prefrontal cortex contributes to working memory remains controversial, as theories differ in their emphasis on its role in storing memories versus controlling their content. To adjudicate between these competing ideas, we tested how perturbations to the human (both sexes) lateral prefrontal cortex impact the storage and control aspects of working memory during a task that requires human subjects to allocate resources to memory items based on their behavioral priority. Our computational model made a strong prediction that disruption of this control process would counterintuitively improve memory for low-priority items. Remarkably, transcranial magnetic stimulation of retinotopically-defined superior precentral sulcus, but not intraparietal sulcus, unbalanced the prioritization of resources, improving memory for low-priority items as predicted by the model. Therefore, these results provide direct causal support for models in which the prefrontal cortex controls the allocation of resources that support working memory, rather than simply storing the features of memoranda.

Efficient Synthesis and Crystal Structure of the HCO⁺ Cation

N₂O Activation and NO Adsorption Control the Simultaneous Conversion of N₂O and NO Using NH₃ over Fe-ZSM-5

Mixed 1D/0D Structures of Chiral Hybrid Lead Halides with an <scp>l</scp>-Nicotinium Spacer Exhibit Broadband Photoluminescence and Polarized Emission

Not So Bioorthogonal Chemistry

Did Mars harbour life? One of the strongest signs yet is spotted in a peculiar rock

Self-Triggering a Locally Alkaline Microenvironment of Co₄Fe₆ for Highly Efficient Neutral Ammonia Electrosynthesis

Internal and External Pockets in Pillar[<i>n</i>]arene Sheets and Their Host–Guest Binding Beyond Cavity Volume Limitations

So you’ve made a lab website. What should go on it?

Generation of Stereocenters via Single-Carbon-Atom Doping Using <i>N</i> -Isocyanides

Monodentate σ-Accepting Boron-Based Ligands Bearing Square-Planar Ni(0) Centers

Does Amplitude Compression Help or Hinder Attentional Neural Speech Tracking?

Amplitude compression is an indispensable feature of contemporary audio production and especially relevant in modern hearing aids. The cortical fate of amplitude-compressed speech signals is not well studied, however, and may yield undesired side effects: We hypothesize that compressing the amplitude envelope of continuous speech reduces neural tracking. Yet, leveraging such a “compression side effect” on unwanted, distracting sounds could potentially support attentive listening if effectively reducing their neural tracking. In this study, we examined 24 young normal hearing (NH) individuals, 19 older hearing-impaired (HI) individuals, and 12 older normal hearing individuals. Participants were instructed to focus on one of two competing talkers while ignoring the other. Envelope compression (1:8 ratio, loudness-matched) was applied to one or both streams containing short speech repeats. Electroencephalography allowed us to quantify the cortical response function and degree of speech tracking. With compression applied to the attended target stream, HI participants showed reduced behavioral accuracy, and compressed speech yielded generally lowered metrics of neural tracking. Importantly, we found that compressing the ignored stream resulted in a stronger neural representation of the uncompressed target speech. Our results imply that intelligent compression algorithms, with variable compression ratios applied to separated sources, could help individuals with hearing loss suppress distraction in complex multitalker environments.

Catalyst-Controlled Regiodivergent Oxidation of Unsymmetrical Diols

Highly Conductive Chiral Organic Cages and Their Helical Assemblies Enable Efficient Spin Filtering

Local Regulation of Striatal Dopamine Release Shifts from Predominantly Cholinergic in Mice to GABAergic in Macaques

Dopamine critically regulates neuronal excitability and promotes synaptic plasticity in the striatum, thereby shaping network connectivity and influencing behavior. These functions establish dopamine as a key neuromodulator, whose release properties have been well studied in rodents but remain understudied in nonhuman primates. This study aims to close this gap by investigating the properties of dopamine release in macaque striatum and comparing/contrasting them to better-characterized mouse striatum, using ex vivo brain slices from male and female animals. Using combined electrochemical techniques and photometry with fluorescent dopamine sensors, we found that evoked dopamine signals have smaller amplitudes in macaques compared with those in mice. Interestingly, cholinergic-dependent dopamine release, which accounts for two-thirds of evoked dopamine release in mouse slices, is significantly reduced in macaques, providing a potential mechanistic underpinning for the observed species difference. In macaques, only nicotinic receptors with alpha-6 subunits contribute to evoked dopamine release, whereas in mice, both alpha-6 and non-alpha6-containing receptors are involved. We also identified robust potentiation of dopamine release in both species when GABA A and GABA B receptors were blocked. This potentiation was stronger in macaques, with an average increase of 50%, compared with 15% in mice. Together, these results suggest that dopamine release in macaque is under stronger GABA-mediated inhibition and that weaker cholinergic-mediated dopamine release may account for the smaller amplitude of evoked dopamine signals in macaque slices.

Lignocellulolytic Bacterial Engineering for Tailoring the Microstructure of Hard Carbon as a Sodium-Ion Battery Anode with Fast Plateau Kinetics

Pallidothalamic Circuit-Selective Manipulation Ameliorates Motor Symptoms in a Rat Model of Parkinsonian

Deep brain stimulation (DBS) effectively treats motor symptoms of advanced Parkinson's disease (PD), with the globus pallidus interna (GPi) commonly targeted. However, its therapeutic mechanisms remain unclear. We employed optogenetic stimulation in the entopeduncular nucleus (EP), the rat homolog of GPi, in a unilateral 6-hydroxydopamine lesioned female Sprague Dawley rat model of PD. We quantified behavioral effects of optogenetic EP DBS on motor symptoms and conducted single-unit recordings in EP and ventral lateral motor thalamus (VL) to examine changes in neural activity. High-frequency optogenetic EP DBS (75, 100, 130 Hz) reduced ipsilateral turning and corrected forelimb stepping, while low-frequency stimulation (5 and 20 Hz) had no effect. EP and VL neurons exhibited mixed response during stimulation, with both increased and decreased firing. The average firing rate of all recorded neurons in the EP and VL significantly increased at 130 Hz but not at other frequencies. Beta-band oscillatory activity was reduced in most EP neurons across high frequencies (75, 100, 130 Hz), while reductions in beta-band oscillations in VL occurred only at 130 Hz. These findings suggest that the neural firing rates within EP and VL circuits were differentially modulated by EP DBS; they may not fully explain the frequency-dependent behavioral effect. Instead, high-frequency optogenetic EP DBS at 130 Hz may ameliorate parkinsonian motor symptoms by reducing abnormal oscillatory activity in the EP–VL circuits. This study underscores the therapeutic potential of circuit-specific modulation in the pallidothalamic pathway using optogenetic EP DBS to alleviate motor deficits in a PD rat model.

Quantum Dynamics of Charge Carriers in Fullerenes Encapsulated by Covalent Organic Polyhedra: Choice of Fullerene Matters

Daily briefing: Saturn has 128 new moons