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BACKGROUND: Chronic stress-induced neuroinflammation plays a pivotal role in the development and exacerbation of mental disorders, such as anxiety and depression. Dimethyl Fumarate (DMF), an effective therapeutic agent approved for the treatment of multiple sclerosis, has been widely reported to display anti-inflammatory and anti-oxidative effects. However, the impact of DMF on chronic stress-induced anxiety disorders and the exact underlying mechanisms remain largely unknown. METHODS: We established a mouse model of chronic social defeat stress (CSDS). DMF was administered orally 1 h before daily stress session for 10 days in CSDS + DMF group. qRT-PCR and western blotting were used to analyze mRNA and protein expression of NLRP3, Caspase-1 and IL-1ß. Immunofluorescence staining was carried out to detect the expression of Iba 1 and c-fos positive cells as well as morphological change of Iba 1+ microglia. Whole-cell patch-clamp recording was applied to evaluate synaptic transmission and intrinsic excitability of neurons. RESULTS: DMF treatment significantly alleviated CSDS-induced anxiety-like behaviors in mice. Mechanistically, DMF treatment prevented CSDS-induced neuroinflammation by inhibiting the activation of microglia and NLRP3/Caspase-1/IL-1ß signaling pathway in basolateral amygdala (BLA), a brain region important for emotional processing. Furthermore, DMF treatment effectively reversed the CSDS-caused disruption of excitatory and inhibitory synaptic transmission balance, as well as the increased intrinsic excitability of BLA neurons. CONCLUSIONS: Our findings provide new evidence that DMF may exert anxiolytic effect by preventing CSDS-induced activation of NLRP3/Caspase-1/IL-1ß signaling pathway and alleviating hyperactivity of BLA neurons.
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Ansiedad , Dimetilfumarato , Ratones Endogámicos C57BL , Proteína con Dominio Pirina 3 de la Familia NLR , Neuronas , Estrés Psicológico , Animales , Dimetilfumarato/farmacología , Dimetilfumarato/uso terapéutico , Masculino , Estrés Psicológico/tratamiento farmacológico , Estrés Psicológico/inmunología , Ratones , Ansiedad/tratamiento farmacológico , Neuronas/efectos de los fármacos , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Amígdala del Cerebelo/efectos de los fármacos , Amígdala del Cerebelo/metabolismo , Enfermedades Neuroinflamatorias/tratamiento farmacológico , Enfermedades Neuroinflamatorias/inmunología , Modelos Animales de Enfermedad , Interleucina-1beta/metabolismo , Microglía/efectos de los fármacos , Conducta Animal/efectos de los fármacos , Caspasa 1/metabolismo , Antiinflamatorios/uso terapéutico , Antiinflamatorios/farmacología , Transducción de Señal/efectos de los fármacos , Derrota SocialRESUMEN
Chloroxylenol is a commonly used antimicrobial agent in antibacterial and disinfection products, which has been detected in various environments, such as wastewater treatment plants, rivers, seawater, and even drinking water, with concentrations ranging from ng/L to mg/L. However, the biodegradation of chloroxylenol received limited attention with only sporadic reports available so far. In this study, an efficient chloroxylenol-degrading consortium, which could degrade 20 mg/L chloroxylenol within two days, was obtained after five months of enrichment. Amplicon sequencing analysis revealed a decrease in the α-diversity (e.g., Shannon index and Inv_Simpson index) of the community during the domestication process. Microbial community dynamics were uncovered, with sequences affiliated to Achromobacter, Pseudomonas, and Rhodococcus identified as the most abundant taxonomic groups. From the consortium, five pure isolates were obtained; however, it was found that only one strain of Rhodococcus could degrade chloroxylenol. Strain Rhodococcus sp. DMU2021 could degrade chloroxylenol efficiently under the conditions of temperature 30-40 °C, and neutral/alkaline conditions. Chloroxylenol was toxic to strain DMU2021 and triggered both enzymatic and non-enzymatic antioxidant systems in response. This study provides novel insights into the biodegradation process of chloroxylenol, as well as valuable bioresources for bioremediation.
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Achromobacter , Rhodococcus , Xilenos , Biodegradación Ambiental , AntibacterianosRESUMEN
Sodium-ion batteries (SIBs) and sodium-ion capacitors (SICs) are promising candidates for cost-effective and large-scale energy storage devices. However, sluggish kinetics and low capacity of traditional anode materials inhibit their practical applications. Herein, a novel design featuring a layer-expanded MoS2 is presented that dual-reinforced by hollow N, P-codoped carbon as the inner supporter and surface groups abundant MXene as the outer supporter, resulting in a cross-linked robust composite (NPC@MoS2 /MXene). The hollow N, P-codoped carbon effectively prevents agglomeration of MoS2 layers and facilitates shorter distances between the electrolyte and electrode. The conductive MXene outer surface envelops the NPC@MoS2 units inside, creating interconnected channels that enable efficient charge transfer and diffusion, ensuring rapid kinetics and enhanced electrode utilization. It exhibits a high reversible capacity of 453 mAh g-1 , remarkable cycling stability, and exceptional rate capability with 54% capacity retention when the current density increases from 100 to 5000 mA g-1 toward SIBs. The kinetic mechanism studies reveal that the NPC@MoS2 /MXene demonstrates a pseudocapacitance dominated hybrid sodiation/desodiation process. Coupled with active carbon (AC), the NPC@MoS2 /MXene//AC SICs achieve both high energy density of 136 Wh kg-1 at 254 W kg-1 and high-power density of 5940 W kg-1 at 27 Wh g-1 , maintaining excellent stability.
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One of the most sought-after topics in neuroscience is to understand how the environment regulates the activity and function of neural circuitry and subsequently influences relevant behaviors. In response to alterations in the environment, the neural circuits undergo adaptive changes ranging from gene expression changes to altered cellular function. Performing sequencing of the transcriptome involved in these behavior-related circuits will provide clues to accurately dissect the detailed mechanisms of related behavior. Here, we describe methods for marking and collecting the ventral hippocampus-projecting basolateral amygdala neurons, which have been repeatedly implicated in regulation of anxiety-like behavior, and subsequently constructing a library ready for sequencing. Specifically, the reported approaches include adeno-associated virus injection, acute brain slice isolation, cell suspension preparation, cell extraction, and cDNA library construction. By utilizing the techniques described here, researchers can comprehensively investigate the transcriptional levels of neural clusters embedded in particular circuits and discover potential pathogenic and therapeutic targets for behavior-relevant disorders. © 2023 Wiley Periodicals LLC. Basic Protocol 1: Tagging of behavior-related neural circuits Basic Protocol 2: Isolation and capture of fluorescent-positive cells Basic Protocol 3: Foundation of sequencing library.
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Amígdala del Cerebelo , Complejo Nuclear Basolateral , Amígdala del Cerebelo/fisiología , Complejo Nuclear Basolateral/fisiología , Neuronas/fisiología , Ansiedad , Análisis de Secuencia de ARNRESUMEN
BACKGROUND: Chronic stress exposure increases the risk of mental health problems such as anxiety and depression. The medial prefrontal cortex (mPFC) is a hub for controlling stress responses through communicating with multiple limbic structures, including the basolateral amygdala (BLA) and nucleus accumbens (NAc). However, considering the complex topographical organization of the mPFC neurons in different subregions (dmPFC vs. vmPFC) and across multiple layers (Layer II/III vs. Layer V), the exact effects of chronic stress on these distinct mPFC output neurons remain largely unknown. RESULTS: We first characterized the topographical organization of mPFC neurons projecting to BLA and NAc. Then, by using a typical mouse model of chronic restraint stress (CRS), we investigated the effects of chronic stress on the synaptic activity and intrinsic properties of the two mPFC neuronal populations. Our results showed that there was limited collateralization of the BLA- and NAc-projecting pyramidal neurons, regardless of the subregion or layer they were situated in. CRS significantly reduced the inhibitory synaptic transmission onto the BLA-projecting neurons in dmPFC layer V without any effect on the excitatory synaptic transmission, thus leading to a shift of the excitation-inhibition (E-I) balance toward excitation. However, CRS did not affect the E-I balance in NAc-projecting neurons in any subregions or layers of mPFC. Moreover, CRS also preferentially increased the intrinsic excitability of the BLA-projecting neurons in dmPFC layer V. By contrast, it even caused a decreasing tendency in the excitability of NAc-projecting neurons in vmPFC layer II/III. CONCLUSION: Our findings indicate that chronic stress exposure preferentially modulates the activity of the mPFC-BLA circuit in a subregion (dmPFC) and laminar (layer V) -dependent manner.
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Anxiety is a normal and transitory emotional state that allows the organisms to cope well with the real or perceived threats, while excessive or prolonged anxiety is a key characteristic of anxiety disorders. We have recently revealed that prolonged anxiety induced by chronic stress is associated with the circuit-varying dysfunction of basolateral amygdala projection neurons (BLA PNs). However, it is not yet known whether similar mechanisms also emerge for acute stress-induced, short-lasting increase of anxiety. Here, using a mouse model of acute restraint stress (ARS), we found that ARS mice showed increased anxiety-like behavior at 2 h but not 24 h after stress, and this effect was accompanied by a transient increase of the activity of BLA PNs. Specifically, ex vivo patch-clamp recordings revealed that the increased BLA neuronal activity did not differ among the distinct BLA neuronal populations, regardless of their projection targets being the dorsomedial prefrontal cortex (dmPFC) or elsewhere. We further demonstrated that such effects were mainly mediated by the enhanced presynaptic glutamate release in dmPFC-to-BLA synapses but not lateral amygdala-to-BLA ones. Furthermore, while optogenetically weakening the presynaptic glutamate release in dmPFC-to-BLA synapses ameliorated ARS-induced anxiety-like behavior, strengthening the release increased in unstressed mice. Together, these findings suggest that acute stress causes short-lasting increase in anxiety-like behavior by facilitating synaptic transmission from the prefrontal cortex to the amygdala in a circuit-independent fashion.
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Complejo Nuclear Basolateral , Humanos , Complejo Nuclear Basolateral/fisiología , Corteza Prefrontal/fisiología , Ansiedad/etiología , Trastornos de Ansiedad , GlutamatosRESUMEN
Dysregulated GABAergic inhibition in the amygdala has long been implicated in stress-related neuropsychiatric disorders. However, the molecular and circuit mechanisms underlying the dysregulation remain elusive. Here, by using a mouse model of chronic social defeat stress (CSDS), we observed that the dysregulation varied drastically across individual projection neurons (PNs) in the basolateral amygdala (BLA), one of the kernel amygdala subregions critical for stress coping. While persistently reducing the extrasynaptic GABAA receptor (GABAAR)-mediated tonic current in the BLA PNs projecting to the ventral hippocampus (BLA â vHPC PNs), CSDS increased the current in those projecting to the anterodorsal bed nucleus of stria terminalis (BLA â adBNST PNs), suggesting projection-based dysregulation of tonic inhibition in BLA PNs by CSDS. Transcriptional and electrophysiological analysis revealed that the opposite CSDS influences were mediated by loss- and gain-of-function of δ-containing GABAARs (GABAA(δ)Rs) in BLA â vHPC and BLA â adBNST PNs, respectively. Importantly, it was the lost inhibition in the former population but not the augmentation in the latter population that correlated with the increased anxiety-like behavior in CSDS mice. Virally mediated maintenance of GABAA(δ)R currents in BLA â vHPC PNs occluded CSDS-induced anxiety-like behavior. These findings clarify the molecular substrate for the dysregulated GABAergic inhibition in amygdala circuits for stress-associated psychopathology.
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Amígdala del Cerebelo , Complejo Nuclear Basolateral , Amígdala del Cerebelo/metabolismo , Complejo Nuclear Basolateral/metabolismo , Ansiedad , Interneuronas/metabolismo , Receptores de GABA-A/genética , Ácido gamma-AminobutíricoRESUMEN
Reversible metal electrodeposition (RME) is an emerging and promising method for designing dynamic windows with electrically controllable transmission, excellent color neutrality, and wide dynamic range. Zn is a viable option for metal-based dynamic windows due to its fast switching kinetics and reversibility despite its very negative deposition voltage. In this manuscript, we study the effect of the supporting electrolyte anions for Zn electrodeposition on transparent tin-doped indium oxide. Through systematic additions or removal of components of the electrolytes, we are able to establish a link between the anions and the effectiveness of Zn RME. This insight allows us to design practical two-electrode 25 cm2 Zn dynamic windows that switch to <1% within 20 s. Lastly, we demonstrate that the accumulation of Zn(OH)2 species on the working electrode degrades the optical contrast of Zn windows during long-term cycling. However, the elimination of these species through acid immersion allows the windows to cycle at least 500 times. Reversible Zn electrodeposition in the presence of a polyethylene glycol additive further improves the cycle life to greater than 1000 cycles. Taken together, these studies highlight important design principles for the construction of robust dynamic windows based on Zn RME.
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Extinguishing the previously acquired fear is critical for the adaptation of an organism to the ever-changing environment, a process requiring the engagement of GABAA receptors (GABAARs). GABAARs consist of tens of structurally, pharmacologically, and functionally heterogeneous subtypes. However, the specific roles of these subtypes in fear extinction remain largely unexplored. Here, we observed that in the medial prefrontal cortex (mPFC), a core region for mood regulation, the extrasynaptically situated, δ-subunit-containing GABAARs [GABAA(δ)Rs], had a permissive role in tuning fear extinction in male mice, an effect sharply contrasting to the established but suppressive role by the whole GABAAR family. First, the fear extinction in individual mice was positively correlated with the level of GABAA(δ)R expression and function in their mPFC. Second, knockdown of GABAA(δ)R in mPFC, specifically in its infralimbic (IL) subregion, sufficed to impair the fear extinction in mice. Third, GABAA(δ)R-deficient mice also showed fear extinction deficits, and re-expressing GABAA(δ)Rs in the IL of these mice rescued the impaired extinction. Further mechanistic studies demonstrated that the permissive effect of GABAA(δ)R was associated with its role in enabling the extinction-evoked plastic regulation of neuronal excitability in IL projection neurons. By contrast, GABAA(δ)R had little influence on the extinction-evoked plasticity of glutamatergic transmission in these cells. Altogether, our findings revealed an unconventional and permissive role of extrasynaptic GABAA receptors in fear extinction through a route relying on nonsynaptic plasticity.SIGNIFICANCE STATEMENT The medial prefrontal cortex (mPFC) is one of the kernel brain regions engaged in fear extinction. Previous studies have repetitively shown that the GABAA receptor (GABAAR) family in this region act to suppress fear extinction. However, the roles of specific GABAAR subtypes in mPFC are largely unknown. We observed that the GABAAR-containing δ-subunit [GABAA(δ)R], a subtype of GABAARs exclusively situated in the extrasynaptic membrane and mediating the tonic neuronal inhibition, works oppositely to the whole GABAAR family and promotes (but does not suppress) fear extinction. More interestingly, in striking contrast to the synaptic GABAARs that suppress fear extinction by breaking the extinction-evoked plasticity of glutamatergic transmission, the GABAA(δ)R promotes fear extinction through enabling the plastic regulation of neuronal excitability in the infralimbic subregion of mPFC. Our findings thus reveal an unconventional role of GABAA(δ)R in promoting fear extinction through a route relying on nonsynaptic plasticity.
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Extinción Psicológica , Miedo , Animales , Miedo/fisiología , Masculino , Ratones , Neuronas/metabolismo , Plásticos/metabolismo , Plásticos/farmacología , Corteza Prefrontal/fisiología , Receptores de GABA-A/metabolismo , Ácido gamma-Aminobutírico/farmacologíaRESUMEN
AIMS: Early life stress (ELS) increases the risk of psychiatric diseases such as anxiety disorders and depression in later life. Hyperactivation of the basolateral amygdala (BLA) neurons plays a pivotal role in the pathogenesis of stress-related diseases. However, the functional roles of BLA neurons in ELS-induced anxiety disorders are not completely understood. MAIN METHODS: Mice were subjected to maternal separation (MS) during postnatal days 3 to 21 to mimic ELS. Anxiety-like behavior was tested by open field test (OFT), elevated plus maze (EPM), and novelty suppressed feeding (NSF). Then, c-fos expression, a proxy for neuronal activity, was evaluated by immunofluorescence. Finally, synaptic transmission and intrinsic excitability were measured by whole-cell patch-clamp recordings. KEY FINDINGS: MS significantly increased anxiety-like behavior in adulthood, as indicated by less time spent in the center area of the OFT, less time spent in and fewer entries to the open arms of the EPM, and increased latency to feed in NSF. Mechanistically, MS increased the expression of c-fos in BLA. MS enhanced the excitatory, but not inhibitory, synaptic transmission onto BLA projection neurons (PNs), which was caused by enhanced presynaptic glutamate release. Moreover, MS also markedly increased the intrinsic neuronal excitability of BLA PNs, probably due to the reduced medium afterhyperpolarization (mAHP) in BLA PNs. SIGNIFICANCE: Our results suggest that the changes of neuronal activity and synaptic transmission in the BLA PNs may play a crucial role in ELS-induced anxiety-like behavior, and these findings provide new insights into the pathological mechanisms of stress-related anxiety disorders.
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Ansiedad , Complejo Nuclear Basolateral , Privación Materna , Plasticidad Neuronal , Estrés Psicológico , Animales , Femenino , Masculino , Ratones , Ansiedad/etiología , Complejo Nuclear Basolateral/fisiopatología , Ratones Endogámicos C57BL , Modelos Animales , Neuronas/fisiología , Transmisión SinápticaRESUMEN
Controlling the microstructure and composition of electrodes is crucial to enhance their rate capability and cycling stability for lithium storage. Inspired by the highly interconnected network and good mechanical integrity of an ant-nest architecture, herein, a biomimetic strategy is proposed to enhance the electrochemical performance of Cu2-xSe. After facile carbonization and selenization treatments, the 3D Cu-MOF is successfully transformed into the final ant-nest-like Cu2-xSe@C (AN-Cu2-xSe@C). The AN-Cu2-xSe@C is composed of interconnected Cu2-xSe channels with amorphous carbon coated on the outer surface. The 3D interconnected channels within the AN-Cu2-xSe@C provide fast charge transport pathways and enhanced structural integrity to tolerate the large volume fluctuations of Cu2-xSe during cycling. When applied as the anode for lithium storage, the AN-Cu2-xSe@C shows remarkable electrochemical performance with a high capacity of 1452 mA h g-1 after 1200 cycles at 1.0 A g-1 and 879 mA h g-1 after 2500 cycles at 10.0 A g-1, respectively. Mechanism investigations demonstrate that the AN-Cu2-xSe@C experiences complicated conversion-intercalation co-existence reactions upon cycling. The existence of capacitive behaviour (74%) also contributes to the extended cycling performance. Our work offers a new avenue for designing a high performance electrode using the biomimetic concept.
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Materiales Biomiméticos/química , Cobre/química , Litio/química , Selenio/química , Carbono/química , Suministros de Energía Eléctrica , ElectrodosRESUMEN
Constructing nanostructures with multi-components and delicate architecture exhibits huge potential to improve the lithium storage performance of electrodes. Herein, we report a novel yolk-double-shell structure with complex chemical compositions. Starting with a core-shell structured Co-ZIF@ZnCo-ZIF as a precursor via a simple selenization process, yolk-double-shell polyhedra that assembled by nanosized Co0.85Se@N-doped carbon as the yolk and the first shell and nanosized Co0.85Se@N-doped carbon and ZnSe@N-doped carbon hetero-components as the second shell (marked as Co0.85Se@NC/ZnSe@NC-YDS) are synthesized. Benefiting from their multiple structural advantages, such as high surface area, large pore volume, uniform carbon coating, and intimate heterostructures, Co0.85Se@NC/ZnSe@NC-YDS exhibits high reversible capacity (1047 mA h g-1) and good rate capability for lithium storage. More importantly, even after 3000 cycles at 5.0 A g-1, an impressive reversible capacity of 468 mA h g-1 is retained with no capacity decay. After repeated discharge/charge processes, the integrated yolk-double-shell structure is still reserved, due to its structural and compositional advantages, which contribute to the enhanced rate and cycling performance.
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Rising levels of atmospheric carbon dioxide due to the burning and depletion of fossil fuels is continuously raising environmental concerns about global warming and the future of our energy supply. Renewable energy, especially better utilization of solar energy, is a promising method for CO2 conversion and chemical storage. Research in the solar fuels area is focused on designing novel catalysts and developing new conversion pathways. In this review, we focus on the photocatalytic reduction of CO2 primarily in its neutral pH species of carbonate to formate. The first two-electron photoproduct of carbon dioxide, a case for formate (or formic acid) is made in this review based on its value as; an important chemical feedstock, a hydrogen storage material, an intermediate to methanol, a high-octane fuel and broad application in fuel cells. This review focuses specifically on the following photocatalysts: semiconductors, phthalocyanines as photosensitizers and membrane devices and metal-organic frameworks.
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BACKGROUND: Fear is an adaptive response across species in the face of threatening cues. It can be either innate or learned through postnatal experience. We have previously shown that genetic deletion of both Rap1a and Rap1b, two isoforms of small GTPase Rap1 in forebrain, causes impairment in auditory fear conditioning. However, the specific roles of these two isoforms are not yet known. RESULTS: In the present study, employing mice with forebrain-restricted deletion of Rap1a or Rap1b, we found that they are both dispensable for normal acquisition of fear learning. However, Rap1b but not Rap1a knockout (KO) mice displayed impairment in the retrieval of learned fear. Subsequently, we found that the expression of c-Fos, a marker of neuronal activity, is specifically decreased in prelimbic cortex (PL) of Rap1b KO mice after auditory fear conditioning, while remained unaltered in the amygdala and infralimbic cortex (IL). On the other hand, neither Rap1a nor Rap1b knockout altered the innate fear of mice in response to their predator odor, 2,5-Dihydro-2,4,5-Trimethylthiazoline (TMT). CONCLUSION: Thus, our results indicate that it is Rap1b but not Rap1a involved in the retrieval process of fear learning, and the learned but not innate fear requires Rap1 signaling in forebrain.
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Chronic or prolonged exposure to stress ranks among the most important socioenvironmental factors contributing to the development of neuropsychiatric diseases, a process generally associated with loss of inhibitory tone in amygdala. Recent studies have identified distinct neuronal circuits within the basolateral amygdala (BLA) engaged in different emotional processes. However, the potential circuit involved in stress-induced dysregulation of inhibitory tones in BLA remains elusive. Here, a transgenic mouse model expressing yellow fluorescent protein under control of the Thy1 promoter was used to differentiate subpopulations of projection neurons (PNs) within the BLA. We observed that the tonic inhibition in amygdala neurons expressing and not expressing Thy1 (Thy1+/-) was oppositely regulated by chronic social defeat stress (CSDS). In unstressed control mice, the tonic inhibitory currents were significantly stronger in Thy1- PNs than their Thy1+ counterparts. CSDS markedly reduced the currents in Thy1- projection neurons (PNs), but increased that in Thy1+ ones. By contrast, CSDS failed to affect both the phasic A-type γ-aminobutyric acid receptor (GABAAR) currents and GABABR currents in these two PN populations. Moreover, chronic corticosterone administration was sufficient to mimic the effect of CSDS on the tonic inhibition of Thy1+ and Thy1- PNs. As a consequence, the suppression of tonic GABAAR currents on the excitability of Thy1- PNs was weakened by CSDS, but enhanced in Thy1+ PNs. The differential regulation of chronic stress on the tonic inhibition in Thy1+ and Thy1- neurons may orchestrate cell-specific adaptation of amygdala neurons to chronic stress.
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The kinetics of MgO+ + CH4 was studied experimentally using the variable ion source, temperature adjustable selected ion flow tube (VISTA-SIFT) apparatus from 300-600 K and computationally by running and analyzing reactive atomistic simulations. Rate coefficients and product branching fractions were determined as a function of temperature. The reaction proceeded with a rate of k = 5.9 ± 1.5 × 10-10(T/300 K)-0.5±0.2 cm3 s-1. MgOH+ was the dominant product at all temperatures, but Mg+, the co-product of oxygen-atom transfer to form methanol, was observed with a product branching fraction of 0.08 ± 0.03(T/300 K)-0.8±0.7. Reactive molecular dynamics simulations using a reactive force field, as well as a neural network trained on thousands of structures yield rate coefficients about one order of magnitude lower. This underestimation of the rates is traced back to the multireference character of the transition state [MgOCH4]+. Statistical modeling of the temperature-dependent kinetics provides further insight into the reactive potential surface. The rate limiting step was found to be consistent with a four-centered activation of the C-H bond, in agreement with previous calculations. The product branching was modeled as a competition between dissociation of an insertion intermediate directly after the rate-limiting transition state, and traversing a transition state corresponding to a methyl migration leading to a Mg-CH3OH+ complex, though only if this transition state is stabilized significantly relative to the dissociated MgOH+ + CH3 product channel. An alternative, non-statistical mechanism is discussed, whereby a post-transition state bifurcation in the potential surface could allow the reaction to proceed directly from the four-centered TS to the Mg-CH3OH+ complex thereby allowing a more robust competition between the product channels.
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Ni-based materials are promising electrocatalysts for the oxygen evolution reaction (OER) for water splitting in alkaline media. We report the synthesis and OER electrocatalysis of both Ni-Cu nanoparticles (20-50 nm in diameter) and Ni-Cu nanoclusters (<20 metal atoms). Analysis of mass spectral data from matrix-assisted laser desorption/ionization and electrospray ionization techniques demonstrates that discrete heterobimetallic Ni-Cu nanoclusters capped with glutathione ligands were successfully synthesized. Ni-Cu nanoclusters with a 52:48 mol % Ni:Cu metal composition display an OER onset overpotential of 50 mV and an overpotential of 150 mV at 10 mA cm-2, which makes this catalyst one of the most efficient nonprecious metal OER catalysts. The durability of the nanocluster catalysts on carbon electrodes can be extended by appending them to electrodes modified with TiO2 nanoparticles. Infrared spectroscopy results indicate that the aggregation dynamics of the glutathione ligands change during catalysis. Taken together, these results help explain the reactivity of a novel class of nanostructured Ni-Cu OER catalysts, which are underexplored alternatives to more commonly studied Ni-Fe, Ni-Co, and Ni-Mn materials.
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The δ subunit-containing GABAA receptor [GABAA(δ)R], which is exclusively situated in the extrasynaptic space, has considerable influence on emotion and behavior. Although the expression of this receptor experiences dramatic fluctuation during postnatal development, it remains unknown whether it regulates emotion in a development-dependent manner. Here, by using mice with genetic deletion of GABAA(δ)R (knockout) and their wild-type littermates, we examined the role of GABAA(δ)R in regulating anxiety-like behavior, as measured with open field test (OFT) and elevated plus maze during the transition from puberty to adulthood. We observed that for female mice, the knockout ones at puberty but not adulthood showed increased anxiety-like behavior in the OFT relative to their wild-type littermates. However, such increase was not observed in elevated plus maze. For male mice, no between-genotype differences were observed in both tests at the above two developmental stages. Our results suggest that GABAA(δ)R preferentially affects the anxiety-like behavior in OFT in a development-dependent manner, but only in female mice.
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Ansiedad/fisiopatología , Receptores de GABA-A/fisiología , Caracteres Sexuales , Factores de Edad , Animales , Femenino , Masculino , Ratones Endogámicos C57BL , Ratones Noqueados , Receptores de GABA-A/genéticaRESUMEN
This article presents the influence of capping ligand and surface interaction types on the coarsening or reshaping behavior of surface-immobilized gold nanoparticles with different core size and shape. The morphological transformation of gold nanoparticles and nanorods on graphene oxide upon heating at temperatures ranging from 50 to 200 °C was investigated. The aggregation and coarsening behaviors of spherical nanoparticles on graphene oxide were slightly affected by the core size of nanoparticles (~ 1, 3, and 10 nm). The comparison of two different surface ligands revealed that glutathione ligands provide much better protection than cetyltrimethylammonium bromide ligands against the morphological transformation of nanoparticles. In addition, the evaluation of surface binding interactions indicated that the attachment of nanoparticles and nanorods onto graphene oxide with additional thiol functional groups could improve the immobilization of particles and therefore decelerate coarsening and reshaping of nanoparticle and nanorods.
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BACKGROUND: Chronic stress exposure increases the risk of developing various neuropsychiatric illnesses. The behavioral sequelae of stress correlate with dendritic hypertrophy and glutamate-related synaptic remodeling at basolateral amygdala projection neurons (BLA PNs). Yet, though BLA PNs are functionally heterogeneous with diverse corticolimbic targets, it remains unclear whether stress differentially impacts specific output circuits. METHODS: Confocal imaging was used to reconstruct the morphology of mouse BLA PNs with the aid of retrograde tracing and biocytin staining. The synaptic activity in these neurons was measured with in vitro electrophysiology, and anxiety-like behavior of the mice was assessed with the elevated plus maze and open field test. RESULTS: Chronic restraint stress (CRS) produced dendritic hypertrophy across mouse BLA PNs, regardless of whether they did (BLAâdorsomedial prefrontal cortex [dmPFC]) or did not (BLAâdmPFC) target dmPFC. However, CRS increased the size of dendritic spine heads and the number of mature, mushroom-shaped spines only in BLAâdmPFC PNs, sparing neighboring BLAâdmPFC PNs. Moreover, the excitatory glutamatergic transmission was also selectively increased in BLAâdmPFC PNs, and this effect correlated with CRS-induced increases in anxiety-like behavior. Segregating BLAâdmPFC PNs based on their targeting of ventral hippocampus (BLAâventral hippocampus) or nucleus accumbens (BLAânucleus accumbens) revealed that CRS increased spine density and glutamatergic signaling in BLAâventral hippocampus PNs in a manner that correlated with anxiety-like behavior. CONCLUSIONS: Chronic stress caused BLA PN neuronal remodeling with a previously unrecognized degree of circuit specificity, offering new insight into the pathophysiological basis of depression, anxiety disorders, and other stress-related conditions.