Summary Proper brain function depends on neurovascular coupling: neural activity rapidly increases local blood flow to meet moment-to-moment changes in regional brain energy demand 1 . Neurovascular coupling is the basis for functional brain imaging 2 , and its impairment is implicated in neurodegeneration 1 . The underlying molecular and cellular mechanisms of neurovascular coupling remain poorly understood. The conventional view is that neurons or astrocytes release vasodilatory factors that act directly on smooth muscle cells (SMC) to induce arterial dilation and increase local blood flow 1 . Here, using two-photon microscopy to image neural activity and vascular dynamics simultaneously in the barrel cortex of awake mice under whisker stimulation, we found that arteriolar endothelial cells (aECs) play an active role in mediating neurovascular coupling. We found that aECs, unlike other vascular segments of ECs in the CNS, have abundant caveolae. Acute genetic perturbations that eliminated caveolae in aECs, but not in neighboring SMCs, impaired neurovascular coupling. Strikingly, caveolae function in aECs is independent of the eNOS-mediated nitric oxide (NO) pathway. Ablation of both caveolae and eNOS completely abolished neurovascular coupling, whereas each single mutant exhibited partial impairment, revealing that caveolae-mediated pathway in aECs is a major contributor to neurovascular coupling. Our findings indicate that vasodilation is largely due to ECs that actively relay signals from the CNS to SMCs via a caveolae-dependent pathway.

Controlling charge transfer at a molecular scale is critical for efficient light harvesting, energy conversion, and nanoelectronics. Dipole-polarization electrets, the electrostatic analogue of magnets, provide a means for "steering" electron transduction via the local electric fields generated by their permanent electric dipoles. Here, we describe the first demonstration of the utility of anthranilamides, moieties with ordered dipoles, for controlling intramolecular charge transfer. Donor− acceptor dyads, each containing a single anthranilamide moiety, distinctly rectify both the forward photoinduced electron transfer and the subsequent charge recombination. Changes in the observed charge-transfer kinetics as a function of media polarity were consistent with the anticipated effects of the anthranilamide molecular dipoles on the rectification. The regioselectivity of electron transfer and the molecular dynamics of the dyads further modulated the observed kinetics, particularly for charge recombination. These findings reveal the underlying complexity of dipole-induced effects on electron transfer and demonstrate unexplored paradigms for molecular rectifiers.

This article presents an investigation on the effectiveness of magnesium and its alloys as a novel class of antibacterial and biodegradable materials for ureteral stent applications. Magnesium is a lightweight and biodegradable metallic material with beneficial properties for use in medical devices. Ureteral stent is one such example of a medical device that is widely used to treat ureteral canal blockages clinically. The bacterial colony formation coupled with the encrustation on the stent surface from extended use often leads to clinical complications and contributes to the failure of indwelling medical devices. We demonstrated that magnesium alloys decreased Escherichia coli viability and reduced the colony forming units over a 3-day incubation period in an artificial urine (AU) solution when compared with currently used commercial polyurethane stent. Moreover, the magnesium degradation resulted in alkaline pH and increased magnesium ion concentration in the AU solution. The antibacterial and degradation properties support the potential use of magnesium-based materials for next-generation ureteral stents. Further studies are needed for clinical translation of biodegradable metallic ureteral stents.

The mouse cerebral cortex contains neurons that express choline acetyltransferase (ChAT) and are a potential local source of acetylcholine. However, the neurotransmitters released by cortical ChAT+ neurons and their synaptic connectivity are unknown. We show that the nearly all cortical ChAT+ neurons in mice are specialized VIP+ interneurons that release GABA strongly onto other inhibitory interneurons and acetylcholine sparsely onto layer 1 interneurons and other VIP+/ChAT+ interneurons. This differential transmission of ACh and GABA based on the postsynaptic target neuron is reflected in VIP+/ChAT+ interneuron pre-synaptic terminals, as quantitative molecular analysis shows that only a subset of these are specialized to release acetylcholine. In addition, we identify a separate, sparse population of non-VIP ChAT+ neurons in the medial prefrontal cortex with a distinct developmental origin that robustly release acetylcholine in layer 1. These results demonstrate both cortex-region heterogeneity in cortical ChAT+ interneurons and target-specific co-release of acetylcholine and GABA.