Template-Assisted Synthesis of a Large-Area Ordered Perovskite Nanowire Array for a High-Performance Photodetector.

One-dimensional (1D) organic-inorganic hybrid perovskite nanowires (NWs) with well-defined structures possess superior optical and electrical properties for optoelectronic applications. However, most of the perovskite NWs are synthesized in air, which makes the NWs susceptible to water vapor, resulting in large amounts of grain boundaries or surface defects. Here, a template-assisted antisolvent crystallization (TAAC) method is designed to fabricate CH3NH3PbBr3 NWs and arrays. It is found that the as-synthesized NW array has designable shapes, low crystal defects, and ordered alignment, which is attributed to the sequestration of water and oxygen in air by the introduction of acetonitrile vapor. The photodetector based on the NWs exhibits an excellent response to light illumination. Under the illumination of a 532 nm laser with 0.1 µW and a bias of -1 V, the responsivity and detectivity of the device reach 1.55 A/W and 1.21 × 1012 Jones, respectively. The transient absorption spectrum (TAS) shows a distinct ground state bleaching signal only at 527 nm, which corresponds to the absorption peak induced by the interband transition of CH3NH3PbBr3. Narrow absorption peaks (a few nanometers) indicate that the energy-level structures of CH3NH3PbBr3 NWs only have a few impurity-level-induced transitions leading to additional optical loss. This work provides an effective and simple strategy to achieve high-quality CH3NH3PbBr3 NWs, which exhibit potential application in photodetection.

Fabrication of Transferable and Micro/Nanostructured Superhydrophobic Surfaces Using Demolding and iCVD Processes.

Superhydrophobic surfaces possess enormous potential in various applications on account of their versatile functionalities. However, artificial superhydrophobic surfaces with ultralow solid/liquid adhesion often require complicated structure fabrication and surface fluorination processes. Here, we designed a superhydrophobic surface possessed of micro/nanoscale structures by employing facile and low-cost demolding and initiated chemical vapor deposition (iCVD) processes. The achieved micro/nanostructured superhydrophobic surface has a maximum static contact angle of ∼170°, a roll-off angle and contact angle hysteresis below 1°, ultralow solid/liquid adhesion for water droplets, and maintains excellent superhydrophobicity after exposure to strongly corrosive species, like strong acid/base and salt solutions, for 60 h. This reasonability-designed method of creating the superhydrophobic surface could provide valuable guidelines for the manufacture of transferable superhydrophobic surfaces and facilitate potential applications extending from optoelectronic devices to self-cleaning materials, such as solar cells, windows, and electronic displays.

Increased GABAergic inhibitory function against ischemic long-term potentiation in the CA1 region of the hippocampus.

Potentiation of N-methyl-D-aspartate receptor (NMDAR)-mediated excitatory synaptic plasticity around 1 h after brief exposure to anoxia/aglycemia is called ischemic long-term potentiation (iLTP), which is considered a pathological form of synaptic response during the early phase of ischemic stroke. It is known that GABAergic inhibitory transmission is also an important molecular process involved in synaptic plasticity and learning memory. However, whether GABAergic transmission is involved in iLTP and early-phase plasticity in ischemic stroke remains unknown. In this study, iLTP was found to be induced in the hippocampal Schaffer-collateral pathway by exposure to oxygen glucose deprivation (OGD). Western blot analysis was conducted to analyze excitatory synaptic receptors and inhibitory synaptic receptors following OGD. The ß3 subunit of the GABAA receptor (GABAAR) was markedly reduced, whereas the GluN2B subunit of the NMDAR was increased in the hippocampal area in the OGD group. Using extracellular recording, we demonstrated that application of GABAAR agonist midazolam could abolish the hippocampal iLTP. Moreover, midazolam had no significant effect on the increase in NMDAR subunit GluN2B, but ameliorated the reduction in the ß3 subunit of GABAAR after OGD. In summary, our results indicated that hippocampal GABAAR reduction promoted synaptic potentiation after OGD. Activation of GABAergic inhibitory transmission function could inhibit iLTP; thus, modulation of GABAergic function is a protective treatment method in the acute phase of synaptic plasticity in ischemic stroke.

Blockade of soluble epoxide hydrolase attenuates post-ischemic neuronal hyperexcitation and confers resilience against stroke with TrkB activation.

Inhibition and deletion of soluble epoxide hydrolase (sEH) has been suggested to ameliorate infarction in experimental ischemic stroke possibly via vasoactive epoxyeicosatrienoic acids. However, it is unknown whether the neuroprotective mechanisms involve alteration of post-ischemic neuronal transmission and neurotrophic signaling. We used a permanent middle cerebral artery occlusion (MCAO) model in adult wild-type mice with the sEH inhibitor 12-(3-adamantan-1-yl-ureido)dodecanoic acid (AUDA) post-treatment and in sEH knockout (sEH KO) mice. We found that sensorimotor recovery was significantly enhanced after MCAO in both AUDA-treated and sEH KO mice, with decreased sEH activity and brain infarction. Decreased post-ischemic long-term potentiation (iLTP) was observed in an ex vivo hippocampal oxygen-glucose deprivation model. Tropomyosin receptor kinase B (TrkB) activation, rather than glutamate receptor alteration, was consistently found after the different manipulations. Immunohistochemistry further revealed peri-infarct neuronal TrkB activation and microvasculature augmentation in AUDA-treated and sEH KO mice, suggesting parallel neurovascular enhancement. Mechanistically, pretreatment with a selective TrkB antagonist ANA12 countered the effect of iLTP attenuation induced by sEH deletion ex vivo and abolished the infarct reduction in vivo. Together, the neuroprotective effects of sEH inhibition and gene deletion can both be mediated partially via enhancement of TrkB signaling which attenuated post-ischemic neuroexcitation and neurological deficits.

Central Thalamic Deep-Brain Stimulation Alters Striatal-Thalamic Connectivity in Cognitive Neural Behavior.

Central thalamic deep brain stimulation (CT-DBS) has been proposed as an experimental therapeutic approach to produce consistent sustained regulation of forebrain arousal for several neurological diseases. We investigated local field potentials (LFPs) induced by CT-DBS from the thalamic central lateral nuclei (CL) and the striatum as potential biomarkers for the enhancement of lever-pressing skill learning. LFPs were simultaneously recorded from multiple sites in the CL, ventral striatum (Vstr), and dorsal striatum (Dstr). LFP oscillation power and functional connectivity were assessed and compared between the CT-DBS and sham control groups. The theta and alpha LFP oscillations were significantly increased in the CL and striatum in the CT-DBS group. Furthermore, interhemispheric coherences between bilateral CL and striatum were increased in the theta band. Additionally, enhancement of c-Fos activity, dopamine D2 receptor (Drd2), and α4-nicotinic acetylcholine receptor (α4-nAChR) occurred after CT-DBS treatment in the striatum and hippocampus. CT-DBS strengthened thalamic-striatal functional connectivity, which demonstrates that the inter-regional connectivity enhancement might contribute to synaptic plasticity in the striatum. Altered dopaminergic and cholinergic receptors resulted in modulation of striatal synaptic plasticity's ability to regulate downstream signaling cascades for higher brain functions of lever-pressing skill learning.