A comprehensive review of the current progresses and material advances in perovskite solar cells.

Recently, perovskite solar cells (PSCs) have attracted ample consideration from the photovoltaic community owing to their continually-increasing power conversion efficiency (PCE), viable solution-processed methods, and inexpensive materials ingredients. Over the past few years, the performance of perovskite-based devices has exceeded 25% due to superior perovskite films achieved using low-temperature synthesis procedures along with evolving appropriate interface and electrode-materials. The current review provides comprehensive knowledge to enhance the performance and materials advances for perovskite solar cells. The latest progress in terms of perovskite crystal structure, device construction, fabrication procedures, and challenges are thoroughly discussed. Also discussed are the different layers such as ETLs and buffer-layers employed in perovskite solar-cells, seeing their transmittance, carrier mobility, and band gap potentials in commercialization. Generally, this review delivers a critical assessment of the improvements, prospects, and trials of PSCs.

Solution processed high performance perovskite solar cells based on a silver nanowire-titanium dioxide hybrid top electrode.

Longer silver nanowires (AgNWs) > 50 µm and even 90 µm in length have been produced via a polyol method by just changing the stirring speed at a temperature of 130 °C. As-synthesized longer AgNWs are further utilized to construct transparent conductive AgNWs films by a facile drop-casting technique that attained a sheet resistance of 14.5 Ω sq-1 and transmittance over 85%, which is higher than ITO film. The use of a AgNWs/TiO2 hybrid electrode decreases the sheet resistance to 8.3 Ω sq-1, which is attributed to the enhancement of connections between AgNWs by filling the empty spaces between nanowires and TiO2 nanoparticles. Transparent perovskite solar cells (PSCs) on the basis of these AgNWs and AgNWs/TiO2 hybrid top electrodes were made and examined. Due to the light scattering nature of TiO2 nanoparticles, optical transmittance of the AgNWs/TiO2 hybrid electrode enhances to some extent after the coating of a TiO2 layer. Both cell efficiencies and stability of the PSCs are enhanced by using the AgNWs/TiO2 top electrode. A power conversion efficiency (PCE) of 10.65% was attained for perovskite devices based on only the AgNW electrode with a sheet resistance of 14.5 Ω sq-1. A PCE of 14.53% was achieved after coating with TiO2 nanoparticles, indicating the layer effect of TiO2 coating.

Correction: Solution processed high performance perovskite solar cells based on a silver nanowire-titanium dioxide hybrid top electrode.

[This corrects the article DOI: 10.1039/D2RA06778A.].

MAPbI3 microneedle-arrays for perovskite photovoltaic application.

Methyl-ammonium lead iodide perovskite (MAPbI3) was synthesized in the form of micro-needles via a hydrothermal route at a low temperature of 100 °C in a two-step procedure for the first time. The results exhibit that the amount of the surfactant is crucial for the synthesis of the MAPbI3 nanostructures with well-controlled morphologies. In contrast to bulk MAPbI3, the one-dimensional (1-D) micro-needle perovskite with a diameter of 200 nm showed an improved hole injection from the perovskite to the hole transporting layer (HTL), providing a unique platform at the perovskite/HTL interface. The best performing device employing MAPbI3 perovskite micro-needles yielded stable and hysteresis-free devices with a best power conversion efficiency of (PCEbest) of 17.98%. The current findings highlight the potential of perovskite micro-needles as novel absorber systems and lay the basis for future commercialization.

Enhanced efficiency and stability of perovskite solar cells using polymer-coated bilayer zinc oxide nanocrystals as the multifunctional electron-transporting layer.

A novel polymer-coated ZnO based bilayer electron transporting material is investigated for highly efficiency perovskite solar cells. The bilayer ETM consisting of an upper-layer of ZnO nanosheets and a lower-layer of ZnO nanoparticles demonstrates the averaged power conversion efficiency of 13.11% and a maximum power conversion efficiency of 15.13%, compared to single-layers of nanosheets (power conversion efficiency = 11.73%) and nanoparticles (power conversion efficiency = 11.08%) films. A conformal coating of a polymer such as polyethylenimine on the surface of bilayered film leading to a significant boost in power conversion efficiency upto 16.39%, thanks to the reduced work function, rapid electron transport and better perovskite infiltration into the bilayer electron transporting material.

Solution-processed barium hydroxide modified boron-doped ZnO bilayer electron transporting materials: Toward stable perovskite solar cells with high efficiency of over 20.5.

ZnO as an electron transporting material (ETM) in perovskite solar cells has many benefits, including low temperature processability and high mobility. We explore here for the first time, hysteresis-less mesostructured perovskite solar cells with an incredible steady-state efficiency of 20.62% particularly enhancement of the device stability. We anticipated a device structure consisting of a novel fully-solution-processed and low-temperature barium hydroxide hybridized boron-doped ZnO (B:ZnO) bilayer film as electron transport material (ETM). We modify the design of ETMs with reduced trap states density is very crucial to obtain highly stabilized power conversion efficiency (PCE) and adjustable architectures in perovskite solar cells which should produce an impact on emerging highly efficient devices and their future commercialization.

Low-temperature electrospray-processed SnO2 nanosheets as an electron transporting layer for stable and high-efficiency perovskite solar cells.

Semiconducting metal oxide electron transporting layers (ETLs) with distinct morphologies have the ability to produce the less-hysteric and high efficiency perovskite solar cells (PSCs). Here, for the first time we introduce a viable electrospraying route for one-step deposition of highly mesoporous SnO2 nanosheets, as the ETLs in PSCs with reduces hysteresis, high charge collection efficiency and improved ambient stability. Furthermore, optimization of the interfacial properties between the SnO2 nanosheets and the perovskite absorber layer by the employment of a C60 interlayer consequences in decreasing the charge recombination, better energy level alignment, and significantly improved power conversion efficiency (PCE). Consequently, the efficient PSCs based on C60-modified SnO2 nanosheets ETLs have almost hysteresis-free behavior, with a best PCE of 20.2% thanks to the highly porous nature of nanosheets and better perovskite infiltration. This study reveals that hierarchical SnO2 is a possible ETL for producing low-cost and efficient PSCs with long-term stability.

Altered behavior and neural activity in conspecific cagemates co-housed with mouse models of brain disorders.

The psychosocial environment is one of the major contributors of social stress. Family members or caregivers who consistently communicate with individuals with brain disorders are considered at risk for physical and mental health deterioration, possibly leading to mental disorders. However, the underlying neural mechanisms of this phenomenon remain poorly understood. To address this, we developed a social stress paradigm in which a mouse model of epilepsy or depression was housed long-term (>4weeks) with normal conspecifics. We characterized the behavioral phenotypes and electrophysiologically investigated the neural activity of conspecific cagemate mice. The cagemates exhibited deficits in behavioral tasks assessing anxiety, locomotion, learning/memory, and depression-like behavior. Furthermore, they showed severe social impairment in social behavioral tasks involving social interaction or aggression. Strikingly, behavioral dysfunction remained in the cagemates 4weeks following co-housing cessation with the mouse models. In an electrophysiological study, the cagemates showed an increased number of spikes in medial prefrontal cortex (mPFC) neurons. Our results demonstrate that conspecifics co-housed with mouse models of brain disorders develop chronic behavioral dysfunctions, and suggest a possible association between abnormal mPFC neural activity and their behavioral pathogenesis. These findings contribute to the understanding of the psychosocial and psychiatric symptoms frequently present in families or caregivers of patients with brain disorders.

Rhythmical Photic Stimulation at Alpha Frequencies Produces Antidepressant-Like Effects in a Mouse Model of Depression.

Current therapies for depression consist primarily of pharmacological agents, including antidepressants, and/or psychiatric counseling, such as psychotherapy. However, light therapy has recently begun to be considered as an effective tool for the treatment of the neuropsychiatric behaviors and symptoms of a variety of brain disorders or diseases, including depression. One methodology employed in light therapy involves flickering photic stimulation within a specific frequency range. The present study investigated whether flickering and flashing photic stimulation with light emitting diodes (LEDs) could improve depression-like behaviors in a corticosterone (CORT)-induced mouse model of depression. Additionally, the effects of the flickering and flashing lights on depressive behavior were compared with those of fluoxetine. Rhythmical flickering photic stimulation at alpha frequencies from 9-11 Hz clearly improved performance on behavioral tasks assessing anxiety, locomotor activity, social interaction, and despair. In contrast, fluoxetine treatment did not strongly improve behavioral performance during the same period compared with flickering photic stimulation. The present findings demonstrated that LED-derived flickering photic stimulation more rapidly improved behavioral outcomes in a CORT-induced mouse model of depression compared with fluoxetine. Thus, the present study suggests that rhythmical photic stimulation at alpha frequencies may aid in the improvement of the quality of life of patients with depression.

Gamma oscillation in functional brain networks is involved in the spontaneous remission of depressive behavior induced by chronic restraint stress in mice.

BACKGROUND: Depression is one of the most prevalent mood disorders, and is known to be associated with abnormal functional connectivity in neural networks of the brain. Interestingly, a significant proportion of patients with depression experience spontaneous remission without any treatment. However, the relationship between electroencephalographic (EEG) functional connectivity and the spontaneous remission in depression remains poorly understood. Here, we investigated regional and network brain activity using EEG signals from a chronic restraint stress (CRS)-induced mouse model of depression. After 1 (CRS1W) or 3 weeks (CRS3W) following the cessation of a 4-week-long CRS, mice were subjected to depression-associated behavioral tasks. EEG signals were obtained from eight cortical regions (frontal, somatosensory, parietal, and visual cortices in each hemisphere). RESULTS: The CRS1W group exhibited behavioral dysfunctions in the open field and forced swim tasks, whereas the CRS3W group displayed normal levels of behaviors in those tasks. In a linear correlation analysis, the CRS1W group exhibited increased correlation coefficient values at all frequency bands (delta, 1.5-4; theta, 4-8; alpha, 8-12; beta, 12-30; gamma, 30-80 Hz) compared with the control group. However, the differences in delta- and gamma-frequency bands between the control and CRS1W groups were no longer observed in the CRS3W group. Persistent brain network homology revealed significantly different functional connectivity between the control and CRS1W groups, and it demonstrated a huge restoration of the decreased distances in the gamma-frequency band for the CRS3W group. Moreover, the CRS3W group displayed a similar strength of connectivity among somatosensory and frontal cortices as the control group. CONCLUSION: A mouse model of CRS-induced depression showed spontaneous behavioral remission of depressive behavior. Using persistent brain network homology analysis of EEG signals from eight cortical regions, we found that restoration of gamma activity at the network level is associated with behavioral remission.

TRPM2, a Susceptibility Gene for Bipolar Disorder, Regulates Glycogen Synthase Kinase-3 Activity in the Brain.

Bipolar disorder (BD) is a psychiatric disease that causes mood swings between manic and depressed states. Although genetic linkage studies have shown an association between BD and TRPM2, a Ca(2+)-permeable cation channel, the nature of this association is unknown. Here, we show that D543E, a mutation of Trpm2 that is frequently found in BD patients, induces loss of function. Trpm2-deficient mice exhibited BD-related behavior such as increased anxiety and decreased social responses, along with disrupted EEG functional connectivity. Moreover, the administration of amphetamine in wild-type mice evoked a notable increase in open-field activity that was reversed by the administration of lithium. However, the anti-manic action of lithium was not observed in the Trpm2(-/-) mice. The brains of Trpm2(-/-) mice showed a marked increase in phosphorylated glycogen synthase kinase-3 (GSK-3), a key element in BD-like behavior and a target of lithium. In contrast, activation of TRPM2 induced the dephosphorylation of GSK-3 via calcineurin, a Ca(2+)-dependent phosphatase. Importantly, the overexpression of the D543E mutant failed to induce the dephosphorylation of GSK-3. Therefore, we conclude that the genetic dysfunction of Trpm2 causes uncontrolled phosphorylation of GSK-3, which may lead to the pathology of BD. Our findings explain the long-sought etiologic mechanism underlying the genetic link between Trpm2 mutation and BD. SIGNIFICANCE STATEMENT: Bipolar disorder (BD) is a mental disorder that causes changes in mood and the etiology is still unknown. TRPM2 is highly associated with BD; however, its involvement in the etiology of BD is still unknown. We show here that TRPM2 plays a central role in causing the pathology of BD. We found that D543E, a mutation of Trpm2 frequently found in BD patients, induces the loss of function. Trpm2-deficient mice exhibited mood disturbances and impairments in social cognition. TRPM2 actively regulates the phosphorylation of GSK-3, which is a main target of lithium, a primary medicine for treating BD. Therefore, abnormal regulation of GSK-3 by hypoactive TRPM2 mutants accounts for the pathology of BD, providing the possible link between BD and TRPM2.

Tracing the evolution of multi-scale functional networks in a mouse model of depression using persistent brain network homology.

Many brain diseases or disorders, such as depression, are known to be associated with abnormal functional connectivity in neural networks in the brain. Some bivariate measures of electroencephalography (EEG) for coupling analysis have been used widely in attempts to explain abnormalities related with depression. However, brain network evolution based on persistent functional connections in EEG signals could not be easily unveiled. For a geometrical exploration of brain network evolution, here, we used persistent brain network homology analysis with EEG signals from a corticosterone (CORT)-induced mouse model of depression. EEG signals were obtained from eight cortical regions (frontal, somatosensory, parietal, and visual cortices in each hemisphere). The persistent homology revealed a significantly different functional connectivity between the control and CORT model, but no differences in common coupling measures, such as cross correlation and coherence, were apparent. The CORT model showed a more localized connectivity and decreased global connectivity than the control. In particular, the somatosensory and parietal cortices were loosely connected in the CORT model. Additionally, the CORT model displayed altered connections among the cortical regions, especially between the frontal and somatosensory cortices, versus the control. This study demonstrates that persistent homology is useful for brain network analysis, and our results indicate that the CORT-induced depression mouse model shows more localized and decreased global connectivity with altered connections, which may facilitate characterization of the abnormal brain network underlying depression.

Differential regulation of observational fear and neural oscillations by serotonin and dopamine in the mouse anterior cingulate cortex.

RATIONALE: The aberrant regulation of serotonin (5-HT) and dopamine (DA) in the brain has been implicated in neuropsychiatric disorders associated with marked impairments in empathy, such as schizophrenia and autism. Many psychiatric drugs bind to both types of receptors, and the anterior cingulate cortex (ACC) is known to be centrally involved with empathy. However, the relationship between the 5-HT/DA system in the ACC and empathic behavior is not yet well known. OBJECTIVES: We investigated the role of 5-HT/DA in empathy-like behavior and in the regulation of ACC neural activity. METHODS: An observational fear learning task was conducted following microinjections of 5-HT, DA, 5-HT and DA, methysergide (5-HT receptor antagonist), SCH-23390 (DA D1 receptor antagonist), or haloperidol (DA D2 receptor antagonist) into the mouse ACC. The ACC neural activity influenced by 5-HT and DA was electrophysiologically characterized in vitro and in vivo. RESULTS: The microinjection of haloperidol, but not methysergide or SCH-23390, decreased the fear response of observing mice. The administration of 5-HT and 5-HT and DA together, but not DA alone, reduced the freezing response of observing mice. 5-HT enhanced delta-band activity and reduced alpha- and gamma-band activities in the ACC, whereas DA reduced only alpha-band activity. Based on entropy, reduced complexity of ACC neural activity was observed with 5-HT treatment. CONCLUSIONS: The current results demonstrated that DA D2 receptors in the ACC are required for observational fear learning, whereas increased 5-HT levels disrupt observational fear and alter the regularity of ACC neural oscillations.

Unique behavioral characteristics and microRNA signatures in a drug resistant epilepsy model.

BACKGROUND: Pharmacoresistance is a major issue in the treatment of epilepsy. However, the mechanism underlying pharmacoresistance to antiepileptic drugs (AEDs) is still unclear, and few animal models have been established for studying drug resistant epilepsy (DRE). In our study, spontaneous recurrent seizures (SRSs) were investigated by video-EEG monitoring during the entire procedure. METHODS/PRINCIPAL FINDINGS: In the mouse pilocarpine-induced epilepsy model, we administered levetiracetam (LEV) and valproate (VPA) in sequence. AED-responsive and AED-resistant mice were naturally selected after 7-day treatment of LEV and VPA. Behavioral tests (open field, object exploration, elevated plus maze, and light-dark transition test) and a microRNA microarray test were performed. Among the 37 epileptic mice with SRS, 23 showed significantly fewer SRSs during administration of LEV (n = 16, LEV sensitive (LS) group) or VPA (n = 7, LEV resistant/VPA sensitive (LRVS) group), while 7 epileptic mice did not show any amelioration with either of the AEDs (n = 7, multidrug resistant (MDR) group). On the behavioral assessment, MDR mice displayed distinctive behaviors in the object exploration and elevated plus maze tests, which were not observed in the LS group. Expression of miRNA was altered in LS and MDR groups, and we identified 4 miRNAs (miR-206, miR-374, miR-468, and miR-142-5p), which were differently modulated in the MDR group versus both control and LS groups. CONCLUSION: This is the first study to identify a pharmacoresistant subgroup, resistant to 2 AEDs, in the pilocarpine-induced epilepsy model. We hypothesize that modulation of the identified miRNAs may play a key role in developing pharmacoresistance and behavioral alterations in the MDR group.