Extracellular ATP released from axons is known to assist activity-dependent signaling between neurons and Schwann cells in the peripheral nervous system. Here we report that ATP released from astrocytes as a result of neuronal activity can also modulate central synaptic transmission. In cultures of hippocampal neurons, endogenously released ATP tonically suppresses glutamatergic synapses via presynaptic P2Y receptors, an effect that depends on the presence of cocultured astrocytes. Glutamate release accompanying neuronal activity also activates non-NMDA receptors of nearby astrocytes and triggers ATP release from these cells, which in turn causes homo- and heterosynaptic suppression. In CA1 pyramidal neurons of hippocampal slices, a similar synaptic suppression was also produced by adenosine, an immediate degradation product of ATP released by glial cells. Thus, neuron-glia crosstalk may participate in activity-dependent synaptic modulation.

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Traumatic brain injury (TBI) is one of the leading causes of neurological disability in young adults. Edaravone, a novel synthetic small-molecule free-radical scavenger, has been shown to have a neuroprotective effect in both animal models of cerebral ischemia and stroke patients; however, the underlying mechanism is poorly understood. In this report, we investigated the potential mechanisms of edaravone treatment in a rat model of TBI. TBI was induced in the right cerebral cortex of male adult rats using Feeney's weight-drop method. Edaravone (0.75, 1.5, or 3 mg/kg) or vehicle (normal saline) was intravenously administered at 2 and 12 h after TBI. Edaravone treatment significantly decreased hippocampal CA3 neuron loss, reduced oxidative stress, and decreased neuronal programmed cell death compared to vehicle treatment. The protective effects of edaravone treatment were also related to the pathology of TBI on non-neuronal cells, as edaravone decreased astrocyte and glial activation. Lastly, edaravone treatment significantly reduced the presence of inflammatory cytokines, cerebral edema, blood-brain barrier (BBB) permeability, and, importantly, neurological deficits following TBI. Our results suggest that edaravone exerts a neuroprotective effect in the rat model of TBI. The likely mechanism is via inhibiting oxidative stress, leading to a decreased inflammatory response and glial activation, and thereby reducing neuronal death and improving neurological function.

Catalyst/support interaction plays a vital role in catalysis towards acidic oxygen evolution (OER), and the performance reinforcement is currently interpreted by either strain or electron donation effect. We herein report that these views are insufficient, where the dynamic evolution of the interface under potential bias must be considered. Taking Nb 2 O 5À x supported iridium (Ir/Nb 2 O 5À x ) as a model catalyst, we uncovered the dynamic migration of oxygen species between IrO x and Nb 2 O 5À x during OER. Direct spectroscopic evidence combined with theoretical computation suggests these migrations not only regulate the in situ Ir structure towards boosted activity, but also suppress its overoxidation via spontaneously delivering excessive oxygen from IrO x to Nb 2 O 5À x . The optimized Ir/Nb 2 O 5À x thus demonstrated exceptional performance in scalable water electrolyzers, i.e., only need 1.839 V to attain 3 A cm À 2 (surpassing the DOE 2025 target), and no activity decay during a 2000 h test at 2 A cm À 2 .

Metal Atom Array In article number 2212827, Wei Luo, Xiaopeng Li, and co‐workers present an emerging heterogeneous catalyst named metal array catalyst (MAC). The MACs possess tunable interatomic distance and electronic properties, strong synergy between atoms, and the predictive nature of the atomic arrangement, which serves as a versatile platform for rationally designing active sites with atomic‐level precision.

A 2,6‐dimethyl phenol–dipentene adduct was synthesized from dipentene (DP) and 2,6‐dimethyl phenol, and then a 2,6‐dimethyl phenol–DP epoxy was synthesized from the reaction of the resultant 2,6‐dimethyl phenol–DP adduct and epichlorohydrin. The proposed structures were confirmed by Fourier transform infrared, elemental analysis, mass spectra, NMR spectra, and epoxy equivalent weight titration. The synthesized 2,6‐dimethyl phenol–DP adduct was cured with 4,4‐diamino diphenyl methane, phenol novolac, 4,4‐diamino diphenyl sulfone, and 4,4‐diamino diphenyl ether. The thermal properties of the cured epoxy resins were studied with differential scanning calorimetry, dynamic mechanical analysis, dielectric analysis, and thermogravimetric analysis. These data were compared with those for the bisphenol A epoxy system. The cured 2,6‐dimethyl phenol–DP epoxy exhibited a lower dielectric constant (ca. 3.1), a lower dissipation factor (ca. 0.065), a lower modulus, lower thermal stability (5% degradation temperature = 366–424 °C), and lower moisture absorption (1.21–2.18%) than the bisphenol A system but a higher glass‐transition temperature (ca. 173–222 °C) than that of bisphenol A system. © 2002 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 40: 4084–4097, 2002

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