Faster Decay Kinetics Research Articles

CoSe2 nanocrystals embedded in one-dimensional mesoporous carbon nanofibers as advanced anode for potassium-ion storage

High-performance potassium-ion batteries have received great attention for electrochemical energy storage owing to their low redox potential, abundant natural resources and excellent safety. As an advanced negative material, CoSe2 has been widely investigated for potassium-ion batteries. Unfortunately, the pure CoSe2 anode suffers from the fast capacity decay and sluggish kinetics, preventing its practical application. Herein, we introduce a novel strategy to fabricate the CoSe2 nanoparticles embedded in one-dimensional mesoporous carbon nanofibers (denoted as 1D-CoSe2@CNFs) with superior high-rate property and good cycle stability for the first time. In this designed material, the conductive carbon nanofibers are loaded with CoSe2 particles. The obtained 1D-CoSe2@CNFs anode shows a specific capacity of 706.3 mAh/g at 0.1 A/g and presents a high capacity retention ratio of around 96.3 % at 5 A/g over 400 cycles. Therefore, this fabricated 1D-CoSe2@CNFs nanocomposite can be employed as a novel negative electrode for potassium-ion storage.

Detection of Hypoxia in 2D and 3D Cell Culture Systems Using Genetically Encoded Fluorescent Hypoxia Sensors.

In vivo oxygen availability varies widely between cellular microenvironments, depending on the tissue of origin and its cellular niche. It has long been known that too high or too low oxygen concentrations can act as a biological stressor. Thus, the precise control of oxygen availability should be a consideration for cell culture optimization, especially in the field of three-dimensional (3D) cell culture. In this chapter, we describe a system for visualizing oxygen limitations at a cellular level using human adipose tissue-derived mesenchymal stem cells (hAD-MSCs) that were genetically modified to express a fluorescent hypoxia sensor. This sensor can detect the activation of hypoxia-induced factors (HIF) transcription factors that lead to the expression of the oxygen-independent fluorescent protein, UnaG, at low oxygen concentrations. The response of these hypoxia reporter cells can be evaluated in two-dimensional (2D) and 3D cultivation platforms during exposure to hypoxia (1% O2) and normoxia (21% O2) using fluorescence microscopy and flow cytometry. We show that hypoxia reporter MSCs exhibit a hypoxia-induced fluorescence signal in both 2D and 3D cultivation platforms with fast decay kinetics after reoxygenation, rendering it a valuable tool for studying the cellular microenvironment and regenerative potential of hAD-MSCs in an in vivo-like setting.

Calcium handling maturation and adaptation to increased substrate stiffness in human iPSC-derived cardiomyocytes: The impact of full-length dystrophin deficiency.

Cardiomyocytes differentiated from human induced Pluripotent Stem Cells (hiPSC- CMs) are a unique source for modelling inherited cardiomyopathies. In particular, the possibility of observing maturation processes in a simple culture dish opens novel perspectives in the study of early-disease defects caused by genetic mutations before the onset of clinical manifestations. For instance, calcium handling abnormalities are considered as a leading cause of cardiomyocyte dysfunction in several genetic-based dilated cardiomyopathies, including rare types such as Duchenne Muscular Dystrophy (DMD)-associated cardiomyopathy. To better define the maturation of calcium handling we simultaneously measured action potential and calcium transients (Ca-Ts) using fluorescent indicators at specific time points. We combined micropatterned substrates with long-term cultures to improve maturation of hiPSC-CMs (60, 75 or 90 days post-differentiation). Control-(hiPSC)-CMs displayed increased maturation over time (90 vs 60 days), with longer action potential duration (APD), increased Ca-T amplitude, faster Ca-T rise (time to peak) and Ca-T decay (RT50). The progressively increased contribution of the SR to Ca release (estimated by post-rest potentiation or Caffeine-induced Ca-Ts) appeared as the main determinant of the progressive rise of Ca-T amplitude during maturation. As an example of severe cardiomyopathy with early onset, we compared hiPSC-CMs generated from a DMD patient (DMD-ΔExon50) and a CRISPR-Cas9 genome edited cell line isogenic to the healthy control with deletion of a G base at position 263 of the DMD gene (c.263delG-CMs). In DMD-hiPSC-CMs, changes of Ca-Ts during maturation were less pronounced: indeed, DMD cells at 90 days showed reduced Ca-T amplitude and faster Ca-T rise and RT50, as compared with control hiPSC-CMs. Caffeine-Ca-T was reduced in amplitude and had a slower time course, suggesting lower SR calcium content and NCX function in DMD vs control cells. Nonetheless, the inotropic and lusitropic responses to forskolin were preserved. CRISPR-induced c.263delG-CM line recapitulated the same developmental calcium handling alterations observed in DMD-CMs. We then tested the effects of micropatterned substrates with higher stiffness. In control hiPSC-CMs, higher stiffness leads to higher amplitude of Ca-T with faster decay kinetics. In hiPSC-CMs lacking full-length dystrophin, however, stiffer substrates did not modify Ca-Ts but only led to higher SR Ca content. These findings highlighted the inability of dystrophin-deficient cardiomyocytes to adjust their calcium homeostasis in response to increases of extracellular matrix stiffness, which suggests a mechanism occurring during the physiological and pathological development (i.e. fibrosis).

High capacity MoO2-based anode enabled by 3D carbon in-situ embedment through a green template strategy

MoO2 material has attracted extensive attention as a competitive candidate because of high theoretical capacity and low cost. However, the large volume change and low conductivity and ion diffusivity of the MoO2 during lithium storage process bring about fast capacity decay and sluggish reaction kinetics, seriously impeding the practical application of MoO2 in lithium-ion batteries. Herein, we demonstrate a relatively green and facile strategy to prepare MoO2/C composite to mitigate above issues. Combined multiple characterization results support that this composite is made up of MoO2 nanoparticles with a 3D porous carbon embedment and hence exhibits upgraded structure stability and enhanced reaction kinetics as a lithium-ion battery anode. Consequently, thus MoO2/C composite shows superior performance, revealing 1050 and 707 mAh g−1 after 110 and 100 cycles at 200 and 1000 mA g−1, respectively. Moreover, this work could offer a new insight into aiming of green preparation of advanced MoO2/C-based anodes for lithium-ion batteries.

In situ implanting fine ZnSe nanoparticles into N-doped porous carbon nanosheets as an exposed highly active and long-life anode for lithium-ion batteries

Owing to the high theoretical specific capacity, transition metal selenides (TMSs) have emerged as promising anode materials for lithium-ion batteries (LIBs). However, the application of TMSs still confronts fast capacity decay and sluggish reaction kinetics associated to their inherent poor conductivity and huge volume expansion during lithiation-delithiation cycles. Herein, the fine ZnSe nanoparticles are implanted into N-doped porous carbon nanosheets through synchronous pyrolysis/selenization of a leaf-like zeolitic imidazolate framework mixed with selenium powder. The highly dispersed fine ZnSe nanoparticles (NPs) coupled with conductive porous carbon nanosheets (denoted as ZnSe/NC) endow the resultant composite with superior structural merits for facilitating electron/ion transfer, thus alleviating the volume fluctuation. The systematic electrochemical investigation illustrates that the as-prepared ZnSe/NC-700 electrode can obtain a high reversible capacity (426.5 mAh g−1 at 1 A g−1 after 1000 cycles), excellent cycling stability (368.9 mAh g−1 after 1800 cycles at 2 A g−1) and nearly 100％ columbic efficiency. In all, our strategy provides a new idea for synthesis of unique anode materials in LIBs.

FRCaMP, a Red Fluorescent Genetically Encoded Calcium Indicator Based on Calmodulin from Schizosaccharomyces Pombe Fungus.

Red fluorescent genetically encoded calcium indicators (GECIs) have expanded the available pallet of colors used for the visualization of neuronal calcium activity in vivo. However, their calcium-binding domain is restricted by calmodulin from metazoans. In this study, we developed red GECI, called FRCaMP, using calmodulin (CaM) from Schizosaccharomyces pombe fungus as a calcium binding domain. Compared to the R-GECO1 indicator in vitro, the purified protein FRCaMP had similar spectral characteristics, brightness, and pH stability but a 1.3-fold lower ΔF/F calcium response and 2.6-fold tighter calcium affinity with Kd of 441 nM and 2.4–6.6-fold lower photostability. In the cytosol of cultured HeLa cells, FRCaMP visualized calcium transients with a ΔF/F dynamic range of 5.6, which was similar to that of R-GECO1. FRCaMP robustly visualized the spontaneous activity of neuronal cultures and had a similar ΔF/F dynamic range of 1.7 but 2.1-fold faster decay kinetics vs. NCaMP7. On electrically stimulated cultured neurons, FRCaMP demonstrated 1.8-fold faster decay kinetics and 1.7-fold lower ΔF/F values per one action potential of 0.23 compared to the NCaMP7 indicator. The fungus-originating CaM of the FRCaMP indicator version with a deleted M13-like peptide did not interact with the cytosolic environment of the HeLa cells in contrast to the metazoa-originating CaM of the similarly truncated version of the GCaMP6s indicator with a deleted M13-like peptide. Finally, we generated a split version of the FRCaMP indicator, which allowed the simultaneous detection of calcium transients and the heterodimerization of bJun/bFos interacting proteins in the nuclei of HeLa cells with a ΔF/F dynamic range of 9.4 and a contrast of 2.3–3.5, respectively.

Live reporting for hypoxia: Hypoxia sensor-modified mesenchymal stem cells as in vitro reporters.

Natural oxygen gradients occur in tissues of biological organisms and also in the context of three-dimensional (3D) in vitro cultivation. Oxygen diffusion limitation and metabolic oxygen consumption by embedded cells produce areas of hypoxia in the tissue/matrix. However, reliable systems to detect oxygen gradients and cellular response to hypoxia in 3D cell culture systems are still missing. In this study, we developed a system for visualization of oxygen gradients in 3D using human adipose tissue-derived mesenchymal stem cells (hAD-MSCs) modified to stably express a fluorescent genetically engineered hypoxia sensor HRE-dUnaG. Modified cells retained their stem cell characteristics in terms of proliferation and differentiation capacity. The hypoxia-reporter cells were evaluated by fluorescence microscopy and flow cytometry under variable oxygen levels (2.5%, 5%, and 7.5% O2 ). We demonstrated that reporter hAD-MSCs output is sensitive to different oxygen levels and displays fast decay kinetics after reoxygenation. Additionally, the reporter cells were encapsulated in bulk hydrogels with a variable cell number, to investigate the sensor response in model 3D cell culture applications. The use of hypoxia-reporting cells based on MSCs represents a valuable tool for approaching the genuine in vivo cellular microenvironment and will allow a better understanding of the regenerative potential of AD-MSCs.

A Missense Mutation A384P Associated with Human Hyperekplexia Reveals a Desensitization Site of Glycine Receptors.

Hyperekplexia, an inherited neuronal disorder characterized by exaggerated startle responses with unexpected sensory stimuli, is caused by dysfunction of glycinergic inhibitory transmission. From analysis of newly identified human hyperekplexia mutations in the glycine receptor (GlyR) α1 subunit, we found that an alanine-to-proline missense mutation (A384P) resulted in substantially higher desensitization level and lower agonist sensitivity of homomeric α1 GlyRs when expressed in HEK cells. The incorporation of the β subunit fully reversed the reduction in agonist sensitivity and partially reversed the desensitization of α1A384P The heteromeric α1A384Pβ GlyRs showed enhanced desensitization but unchanged agonist-induced maximum responses, surface expression, main channel conductance, and voltage dependence compared with that of the wild-type α1β (α1WTβ) GlyRs. Coexpression of the R392H and A384P mutant α1 subunits, which mimic the expression of the compound heterozygous mutation in a hyperekplexia patient, resulted in channel properties similar to those with α1A384P subunit expression alone. In comparison, another human hyperekplexia mutation α1P250T, which was previously reported to enhance desensitization, caused a strong reduction in maximum currents in addition to the altered desensitization. These results were further confirmed by overexpression of α1P250T or α1A384P subunits in cultured neurons isolated from SD rats of either sex. Moreover, the IPSC-like responses of cells expressing α1A384Pβ induced by repeated glycine pulses showed a stronger frequency-dependent reduction than those expressing α1WTβ. Together, our findings demonstrate that A384 is associated with the desensitization site of the α1 subunit and its proline mutation produced enhanced desensitization of GlyRs, which contributes to the pathogenesis of human hyperekplexia.SIGNIFICANCE STATEMENT Human startle disease is caused by impaired synaptic inhibition in the brainstem and spinal cord, which is due to either direct loss of GlyR channel function or reduced number of synaptic GlyRs. Considering that fast decay kinetics of GlyR-mediated inhibitory synaptic responses, the question was raised whether altered desensitization of GlyRs will cause dysfunction of glycine transmission and disease phenotypes. Here, we found that the α1 subunit mutation A384P, identified from startle disease patients, results in enhanced desensitization and leads to rapidly decreasing responses in the mutant GlyRs when they are activated repeatedly by the synaptic-like simulation. These observations suggest that the enhanced desensitization of postsynaptic GlyRs could be the primary pathogenic mechanism of human startle disease.

Luminescent PEO Coatings on Aluminum

Results show the possibilities of pore filling approach to modify alumina coatings with various materials in order to enhance coating optical (or other) properties and develop new functional materials; as well as demonstrate novel alumina phase transition detection approach. Luminescent PEO coatings were produced on aluminum surface using pore-filling method. Three stage process was developed to modify alumina coating in order to enhance its luminescent properties. Eu3+ recharging to Eu2+ followed by significant (up to 10 times) total luminescence intensity increase was observed, Eu ion presence evaluated in final coating by measuring fast decay kinetics. Structure of obtained coatings was analyzed using XRD and FTIR spectroscopy indicating presence of η-alumina phase.

Strychnine-sensitive glycine receptors on pyramidal neurons in layers II/III of the mouse prefrontal cortex are tonically activated.

Processing of signals within the cerebral cortex requires integration of synaptic inputs and a coordination between excitatory and inhibitory neurotransmission. In addition to the classic form of synaptic inhibition, another important mechanism that can regulate neuronal excitability is tonic inhibition via sustained activation of receptors by ambient levels of inhibitory neurotransmitter, usually GABA. The purpose of this study was to determine whether this occurs in layer II/III pyramidal neurons (PNs) in the prelimbic region of the mouse medial prefrontal cortex (mPFC). We found that these neurons respond to exogenous GABA and to the α4δ-containing GABAA receptor (GABA(A)R)-selective agonist gaboxadol, consistent with the presence of extrasynaptic GABA(A)R populations. Spontaneous and miniature synaptic currents were blocked by the GABA(A)R antagonist gabazine and had fast decay kinetics, consistent with typical synaptic GABA(A)Rs. Very few layer II/III neurons showed a baseline current shift in response to gabazine, but almost all showed a current shift (15-25 pA) in response to picrotoxin. In addition to being a noncompetitive antagonist at GABA(A)Rs, picrotoxin also blocks homomeric glycine receptors (GlyRs). Application of the GlyR antagonist strychnine caused a modest but consistent shift (∼15 pA) in membrane current, without affecting spontaneous synaptic events, consistent with the tonic activation of GlyRs. Further investigation showed that these neurons respond in a concentration-dependent manner to glycine and taurine. Inhibition of glycine transporter 1 (GlyT1) with sarcosine resulted in an inward current and an increase of the strychnine-sensitive current. Our data demonstrate the existence of functional GlyRs in layer II/III of the mPFC and a role for these receptors in tonic inhibition that can have an important influence on mPFC excitability and signal processing.

The Cooperation of Sustained and Phasic Inhibitions Increases the Contrast of ITD-Tuning in Low-Frequency Neurons of the Chick Nucleus Laminaris

Neurons in the nucleus laminaris (NL) of birds detect the coincidence of binaural excitatory inputs from the nucleus magnocellularis (NM) on both sides and process the interaural time differences (ITDs) for sound localization. Sustained inhibition from the superior olivary nucleus is known to control the gain of coincidence detection, which allows the sensitivity of NL neurons to ITD tolerate strong-intensity sound. Here, we found a phasic inhibition in chicken brain slices that follows the ipsilateral NM inputs after a short time delay, sharpens coincidence detection, and may enhance ITD sensitivity in low-frequency NL neurons. GABA-positive small neurons are distributed in and near the NL. These neurons generate IPSCs in NL neurons when photoactivated by a caged glutamate compound, suggesting that these GABAergic neurons are interneurons that mediate phasic inhibition. These IPSCs have fast decay kinetics that is attributable to the α1-subunit of the GABAA receptor, the expression of which dominates in the low-frequency region of the NL. Model simulations demonstrate that phasic IPSCs narrow the time window of coincidence detection and increase the contrast of ITD-tuning during low-level, low-frequency excitatory input. Furthermore, cooperation of the phasic and sustained inhibitions effectively increases the contrast of ITD-tuning over a wide range of excitatory input levels. We propose that the complementary interaction between phasic and sustained inhibitions is the neural mechanism that regulates ITD sensitivity for low-frequency sound in the NL.

Effects of arsenic on growth and photosystem II (PSII) activity of Microcystis aeruginosa

Effects of arsenic on growth, pigments content, oxygen evolution and photosystem II (PSII) activity of Microcystis aeruginosa were investigated in the present study. Various concentrations of As(III) did not show significant effects on growth and total carotenoids content within 24h of treatment. After 48h of treatment, 10mgL−1 As(III) significantly inhibited the growth and synthesis of carotenoids of M. aeruginosa, while As(III) at concentrations ranging from 0 to 1mgL−1 showed no significant inhibition. Chlorophyll a synthesis, oxygen evolution and chlorophyll fluorescence were more sensitive to As(III) exposure than carotenoid synthesis and growth. Chlorophyll a content, fast fluorescence rise transients and fluorescence decay kinetics appeared to be affected after the cells were exposed to 1 and 10mgL−1 As(III) for more than 24h. Treatment with 10mgL−1 As(III) for 24h or longer led to flattening of the fluorescence transient and drastic decrease of amplitude of fast phase of QA− reoxidation kinetics. Exposure to As(III) mainly inhibited the quantum yield for primary photochemistry, density of reaction centers and photosynthesis performance index, and increased the dissipated energy. The decrease in amplitude of the fast and middle phases further revealed that once electron transfer from QA− to QB was inhibited by As(III), more QA− was reoxidized via S2(QAQB)− charge recombination. As(III) stress may result in an increased stability of the S2QB− and S2QA− recombination.

Absorption and luminescence in amorphous SixGe1-xO2 films fabricated by SPCVD

Optical absorption and photoluminescence of Ge-doped silica films fabricated by the surface-plasma chemical vapor deposition (SPCVD) are studied in the 2–8eV spectral band. The deposited on silica substrate films of about 10μm in thickness are composed as x·GeO2-(1-x)·SiO2 with x ranging from 0.02 to 1. It is found that all as‐deposited films do not luminesce under the excitation by a KrF (5eV) excimer laser, thus indicating lack of oxygen deficient centers (ODCs) in them. After subsequent fusion of silicon containing (x<1) films by a scanning focused CO2 laser beam absorption band centered at 5eV as well as two luminescence bands centered at blue (3.1eV) and UV (4.3eV) wavelengths arise, highlighting the formation of the ODCs. The excitation of unfused SPCVD films by an ArF (6.4eV) excimer laser yields a luminescence spectrum with two bands typical for the ODCs, but with a faster decay kinetics. Intensities of these bands grow up with samples cooling down to a temperature of 80–60K. Unfused films excited by the ArF laser also demonstrate luminescence due to recombination of a trapped charge resulted from the excitation of localized electron states of the glass network. In the unfused GeO2 film luminescence related to a self-trapped exciton (STE) typical for GeO2 crystals with α-quartz structure is observed. The observed STE luminescence can be indicative of the crystalline fraction availability in the film. Whereas GeO2 crystals are known as not containing twofold coordinated germanium, a polycrystalline inclusion in the SPCVD GeO2 film serves as a factor explaining the absence of any spectroscopic manifestation of this type of defects in it even after fusion. On the other hand, lack of STE luminescence in other unfused films with x<1 testifies truly amorphous state of the matter in them.

Concentration dependence study of VUV–UV–visible luminescence of Nd3+ and Gd3+ in LuLiF4

An overview of absorption and luminescence characteristics of Nd3+ and Gd3+ centers in a LiLuF4 single crystal host is provided. Single crystals doped with the above rare earth ions were prepared by micro-pulling-down technique in the form of rods a few cm long with a diameter of about 2mm. Excitation and emission spectra and fast decay kinetics in VUV and UV spectral regions were measured at room temperature. The observed absorption and emission peaks are due to the 5d–4f and 4f–4f optical transitions of Nd3+ and Gd3+ centers. Concentration dependence of the decay kinetics is also discussed.

Stochastic signalling rewires the interaction map of a multiple feedback network during yeast evolution

During evolution, genetic networks are rewired through strengthening or weakening their interactions to develop new regulatory schemes. In the galactose network, the GAL1/GAL3 paralogues and the GAL2 gene enhance their own expression mediated by the Gal4p transcriptional activator. The wiring strength in these feedback loops is set by the number of Gal4p binding sites. Here we show using synthetic circuits that multiplying the binding sites increases the expression of a gene under the direct control of an activator, but this enhancement is not fed back in the circuit. The feedback loops are rather activated by genes that have frequent stochastic bursts and fast RNA decay rates. In this way, rapid adaptation to galactose can be triggered even by weakly expressed genes. Our results indicate that nonlinear stochastic transcriptional responses enable feedback loops to function autonomously, or contrary to what is dictated by the strength of interactions enclosing the circuit.

Dynamics of exciton creation and decay processes in composition – disordered InGaN thin films

In the GaN-based ternary alloys, InGaN crystals have been recognized as key materials for e-h plasmas-exciton dynamics, because of large exciton binding energies (24.8 meV in GaN). We report investigations of creating and recombination dynamics of excitons in commercially important InxGa1-xN composition range from x = 0.1 to 0.18 in which nanoscale indium composition fluctuation occurs and formation of indium rich clusters acting as quantum dots (QD) can be expected. Three MOCVD grown samples having x = 0.1; 0.14 and 0.18 have been investigated using 3D picosecond transient PL spectroscopy. It has been found that the band to band photo excitation at 15 K in whole composition range results in creating of complex luminescence band represented by three close overlapping Gaussian shape single exciton bands. All three exciton bands show fast decay time constants in a picosecond range. For all the samples the PL intensity dependence on excitation pulse power for each exciton band is different. An increase of the excitation pulse power density results in the linear growth of the band at the higher photon energy side. The next energy bands with lower photon energy show correspondingly quadratic and cubic dependences on laser pulse energy and are caused by the formation of biexcitons and triexcitons. Fast decay kinetics and excitation of multi-excitonic complexes are evident for important role of quantum dots by quantum capture of excitons in the considered composition range.

Slowing of Instantaneous Inactivation Causes Macroscopic Current Decay in Kv7.1 Alanine Mutants

Alanine scanning mutagenesis in Kv7.1 S4-S5 linker and the pore region revealed mutant channels with fast current decay at permanent depolarizing pulses above 10mV. It has been previously shown that such a macroscopic inactivation of many Kv7.1 pore mutants occurs in parallel to instantaneous inactivation of Kv7.1 channel. We have chosen four mutant channels I268A, G269A, F339A and F340A with most pronounced current decays to investigate the molecular mechanism underling decay process. Inactivation of these channels could not be explained by intracellular Na+ block reported earlier for Kv7.1 wild type channel. The fast current decay kinetics significantly changed neither by varying the extracellular K+ concentration nor by replacement of the K+ with equimolar Rb+. Recovery from inactivation showed fast and slow components. The slow component was accelerated at high extracellular K+ conditions, whereas the fast component did not change significantly. Our data suggest that instantaneous inactivation of wild type Kv7.1 channel markedly slowed by above mentioned alanine mutations resulting in macroscopic decay of current during prolonged depolarization.

VUV-UV-visible luminescence of Nd3+, Er3+ and Tm3+ and energy distribution in LiLuF4 single crystal host

It is the aim of this contribution to provide an overview of luminescence spectra and decay characteristics of Nd3+, Er3+ and Tm3+ centers in LiLuF4 single crystal including possible energy transfer mechanisms towards and away from the Nd3+ 5d excited state. Single crystal doped with the mentioned RE ions were prepared by micro-pulling-down technique. Excitation and emission spectra and fast decay kinetics in VUV spectral region are completed with radio-and photoluminescence spectra and decay kinetics in UV-visible region.

VUV-UV-visible luminescence of Nd3+, Er3+ and Tm3+ in LiLuF4 single crystal host

Abstract An overlook of absorption and luminescence characteristics of Nd3+, Er3+ and Tm3+ centers in LiLuF4 single crystal is provided. Single crystal doped with the mentioned RE ions were prepared by micro-pulling-down technique in the form of few cm long rods with the diameter of about 2 mm. Excitation and emission spectra and fast decay kinetics in VUV spectral region were measured at SUPERLUMI station at synchrotron DESY, Hamburg and characterization was further completed in UV-visible region at conventional spectrophotometers. Observed absorption and emission peaks are ascribed to the 5d–4f and 4f–4f optical transitions in the doped rare earth ions. Concentration dependence of the decay kinetics is discussed.

Excitatory and Inhibitory Synapses in Neuropeptide Y–Expressing Striatal Interneurons

Although rare, interneurons are pivotal in governing striatal output by extensive axonal arborizations synapsing on medium spiny neurons. Using a genetically modified mouse strain in which a green fluorescent protein (GFP) is driven to be expressed under control of the neuropeptide Y (NPY) promoter, we identified NPY interneurons and compared them with striatal principal neurons. We found that the bacteria artificial chromosome (BAC)-npy mouse expresses GFP with high fidelity in the striatum to the endogenous expression of NPY. Patch-clamp analysis from NPY neurons showed a heterogeneous population of striatal interneurons. In the majority of cells, we observed spontaneous firing of action potentials in extracellular recordings. On membrane rupture, most NPY interneurons could be classified as low-threshold spiking interneurons and had high-input resistance. Voltage-clamp recordings showed that both GABA and glutamate gated ion channels mediate synaptic inputs onto these striatal interneurons. AMPA receptor-mediated spontaneous excitatory postsynaptic currents (sEPSCs) were small in amplitude and infrequent in NPY neurons. Evoked EPSCs did not show short-term plasticity but some rectification. Evoked N-methyl-d-aspartate (NMDA) EPSCs had fast decay kinetics and were poorly sensitive to an NR2B subunit containing NMDA receptor blocker. Spontaneous inhibitory postsynaptic currents (sIPSCs) were mediated by GABA(A) receptors and were quite similar among all striatal neurons studied. On the contrary, evoked IPSCs decayed faster in NPY neurons than in other striatal neurons. These data report for the first time specific properties of synaptic transmission to NPY striatal interneurons.