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Decay Time Constant (decay + time_constant)
Selected AbstractsThin film formation by rf sputtering with EuGa2S4 target and photoluminescence of the prepared filmsPHYSICA STATUS SOLIDI (C) - CURRENT TOPICS IN SOLID STATE PHYSICS, Issue 8 2006M. Dohi Abstract Thin films were deposited on Si and fused quartz substrates by rf sputtering with EuGa2S4 target. The deposited films were annealed in the mixed atmosphere of S and He, which led crystallization of the film from amorphous phase. Photoluminescence of the annealed films, characteristic to the Eu2+ ion, was observed with room temperature quantum efficiency of 17%. Decay time constants at room temperature and liquid nitrogen temperature were measured to be 140 ns, and 430 ns, respectively. The latter value is close to the reported radiative lifetime of the EuGa2S4 crystal. Construction possibility of a surface-emitting laser is discussed with data on behaviour of excitation intensity dependent time-resolved spectra under pulsed laser excitation and on surface roughness of the film. (© 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] Glycinergic input of widefield, displaced amacrine cells of the mouse retinaTHE JOURNAL OF PHYSIOLOGY, Issue 15 2009Sriparna Majumdar Glycine receptors (GlyRs) of displaced amacrine cells of the mouse retina were analysed using whole cell recordings and immunocytochemical staining with subunit-specific antibodies. During the recordings the cells were filled with a fluorescent tracer and 11 different morphological types could be identified. The studies were performed in wild-type mice and in mutant mice deficient in the GlyR,1 (Glra1spd-ot, ,oscillator' mouse), the GlyR,2 (Glra2,/,) and the GlyR,3 subunit (Glra3,/,). Based on their responses to the application of exogenous glycine in the retinas of wild-type and mutant mice, the cells were grouped into three major classes: group I cells (comprising the morphological types MA-S5, MA-S1, MA-S1/S5, A17, PA-S1, PA-S5 and WA-S1), group II cells (comprising the morphological types PA-S4, WA-S3 and WA-multi) and ON-starburst cells. For further analysis, spontaneous inhibitory postsynaptic currents (sIPSCs) were measured both in wild-type and mutant mouse retinas. Glycinergic sIPSCs and glycine induced currents of group I cells remained unaltered across wild-type and the three mutant mice (mean decay time constant of sIPSCs, ,,25 ms). Group II cells showed glycinergic sIPSCs and glycine induced currents in wild-type, Glra1spd-ot and Glra3,/, mice (,,25 ms); however, glycinergic currents were absent in group II cells of Glra2,/, mice. Glycine induced currents and sIPSCs recorded from ON-starburst amacrine cells did not differ significantly between wild-type and the mutant mouse retinas (,,50,70 ms). We propose that GlyRs of group II cells are dominated by the ,2 subunit; GlyRs of ON-starburst amacrine cells appear to be dominated by the ,4 subunit. [source] Efficient Ca2+ buffering in fast-spiking basket cells of rat hippocampusTHE JOURNAL OF PHYSIOLOGY, Issue 8 2008Yexica Aponte Fast-spiking parvalbumin-expressing basket cells (BCs) represent a major type of inhibitory interneuron in the hippocampus. These cells inhibit principal cells in a temporally precise manner and are involved in the generation of network oscillations. Although BCs show a unique expression profile of Ca2+ -permeable receptors, Ca2+ -binding proteins and Ca2+ -dependent signalling molecules, physiological Ca2+ signalling in these interneurons has not been investigated. To study action potential (AP)-induced dendritic Ca2+ influx and buffering, we combined whole-cell patch-clamp recordings with ratiometric Ca2+ imaging from the proximal apical dendrites of rigorously identified BCs in acute slices, using the high-affinity Ca2+ indicator fura-2 or the low-affinity dye fura-FF. Single APs evoked dendritic Ca2+ transients with small amplitude. Bursts of APs evoked Ca2+ transients with amplitudes that increased linearly with AP number. Analysis of Ca2+ transients under steady-state conditions with different fura-2 concentrations and during loading with 200 ,m fura-2 indicated that the endogenous Ca2+ -binding ratio was ,200 (,S= 202 ± 26 for the loading experiments). The peak amplitude of the Ca2+ transients measured directly with 100 ,m fura-FF was 39 nm AP,1. At ,23°C, the decay time constant of the Ca2+ transients was 390 ms, corresponding to an extrusion rate of ,600 s,1. At 34°C, the decay time constant was 203 ms and the corresponding extrusion rate was ,1100 s,1. At both temperatures, continuous theta-burst activity with three to five APs per theta cycle, as occurs in vivo during exploration, led to a moderate increase in the global Ca2+ concentration that was proportional to AP number, whereas more intense stimulation was required to reach micromolar Ca2+ concentrations and to shift Ca2+ signalling into a non-linear regime. In conclusion, dentate gyrus BCs show a high endogenous Ca2+ -binding ratio, a small AP-induced dendritic Ca2+ influx, and a relatively slow Ca2+ extrusion. These specific buffering properties of BCs will sharpen the time course of local Ca2+ signals, while prolonging the decay of global Ca2+ signals. [source] Accumulation of cytoplasmic calcium, but not apamin-sensitive afterhyperpolarization current, during high frequency firing in rat subthalamic nucleus cellsTHE JOURNAL OF PHYSIOLOGY, Issue 3 2008Mark Teagarden The autonomous firing pattern of neurons in the rat subthalamic nucleus (STN) is shaped by action potential afterhyperpolarization currents. One of these is an apamin-sensitive calcium-dependent potassium current (SK). The duration of SK current is usually considered to be limited by the clearance of calcium from the vicinity of the channel. When the cell is driven to fire faster, calcium is expected to accumulate, and this is expected to result in accumulation of calcium-dependent AHP current. We measured the time course of calcium transients in the soma and proximal dendrites of STN neurons during spontaneous firing and their accumulation during driven firing. We compared these to the time course and accumulation of AHP currents using whole-cell and perforated patch recordings. During spontaneous firing, a rise in free cytoplasmic calcium was seen after each action potential, and decayed with a time constant of about 200 ms in the soma, and 80 ms in the dendrites. At rates higher than 10 Hz, calcium transients accumulated as predicted. In addition, there was a slow calcium transient not predicted by summation of action potentials that became more pronounced at high firing frequency. Spike AHP currents were measured in voltage clamp as tail currents after 2 ms voltage pulses that triggered action currents. Apamin-sensitive AHP (SK) current was measured by subtraction of tail currents obtained before and after treatment with apamin. SK current peaked between 10 and 15 ms after an action potential, had a decay time constant of about 30 ms, and showed no accumulation. At frequencies between 5 and 200 spikes s,1, the maximal SK current remained the same as that evoked by a single action potential. AHP current did not have time to decay between action potentials, so at frequencies above 50 spikes s,1 the apamin-sensitive current was effectively constant. These results are inconsistent with the view that the decay of SK current is governed by calcium dynamics. They suggest that the calcium is present at the SK channel for a very short time after each action potential, and the current decays at a rate set by the deactivation kinetics of the SK channel. At high rates, repetitive firing was governed by a fast apamin-insensitive AHP current that did not accumulate, but rather showed depression with increases in activation frequency. A slowly accumulating AHP current, also insensitive to apamin, was extremely small at low rates but became significant with higher firing rates. [source] Functional segregation of synaptic GABAA and GABAC receptors in goldfish bipolar cell terminalsTHE JOURNAL OF PHYSIOLOGY, Issue 1 2006Mary J. Palmer The transmission of light responses to retinal ganglion cells is regulated by inhibitory input from amacrine cells to bipolar cell (BC) synaptic terminals. GABAA and GABAC receptors in BC terminals mediate currents with different kinetics and are likely to have distinct functions in limiting BC output; however, the synaptic properties and localization of the receptors are currently poorly understood. By recording endogenous GABA receptor currents directly from BC terminals in goldfish retinal slices, I show that spontaneous GABA release activates rapid GABAA receptor miniature inhibitory postsynaptic currents (mIPSCs) (predominant decay time constant (,decay), 1.0 ms) in addition to a tonic GABAC receptor current. The GABAC receptor antagonist (1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA) has no effect on the amplitude or kinetics of the rapid GABAA mIPSCs. In addition, inhibition of the GAT-1 GABA transporter, which strongly regulates GABAC receptor currents in BC terminals, fails to reveal a GABAC component in the mIPSCs. These data suggest that GABAA and GABAC receptors are highly unlikely to be synaptically colocalized. Using non-stationary noise analysis of the mIPSCs, I estimate that GABAA receptors in BC terminals have a single-channel conductance (,) of 17 pS and that an average of just seven receptors mediates a quantal event. From noise analysis of the tonic current, GABAC receptor , is estimated to be 4 pS. Identified GABAC receptor mIPSCs exhibit a slow decay (,decay, 54 ms) and are mediated by approximately 42 receptors. The distinct properties and localization of synaptic GABAA and GABAC receptors in BC terminals are likely to facilitate their specific roles in regulating the transmission of light responses in the retina. [source] Effects of binocular form deprivation on the excitatory post-synaptic currents mediated by N-methyl-D-aspartate receptors in rat visual cortexCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 3 2004Wei Qin MD Abstract Purpose:,To investigate the effects of binocular form deprivation (BFD) on the excitatory post-synaptic currents (EPSCs) mediated by the N-methyl-D-aspartate (NMDA) receptor (NMDA-EPSCs), and the proportion of NMDA-EPSCs relative to glutamate receptor currents (glutamate-EPSCs) in rat visual cortex. Methods:,Binocular form deprivation was achieved by suturing the eyelids of Wistar rats at postnatal day (PD) 14, before eye-opening. Visual cortical slices (300 µm) were prepared from normal and BFD Wistar rats aged PD 14, 21 and 28. Recordings were obtained in slices from layer II to IV using the whole-cell patch-clamp technique. Glutamate-EPSCs were isolated in the presence of bicuculline methiodide (20 µmol/L) in the bathing medium, and NMDA-EPSCs were isolated with a combination of bicuculline methiodide (20 µmol/L) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 20 µmol/L). In addition, D,L-2-amino-5-phosphonovalerate (AP-5, 20 µmol/L) was applied to study the NMDA-only mediated currents. For each cell, the ratio of peak NMDA to glutamate EPSCs was calculated. Results:,During visual development, the decay time constant of NMDA-EPSCs became shorter after eye-opening in normal rats (F = 5.949, P <0.05; PD 28 vs PD 14, P = 0.027), but not in rats with BFD (P > 0.05). The weighted time constant of NMDA-EPSCs in the visual cortex became shorter after the rats' eyes were opened in the normal group (F2,37 = 4.727, P = 0.015; PD 28 vs PD 14, P = 0.035), but not in the BFD group (P > 0.05). However, the rise time constant and peak value of NMDA-EPSCs showed no significant changes in normal and BFD groups (P > 0.05). The ratio of NMDA-EPSCs to glutamate-EPSCs became gradually smaller with age in the normal rats (F = 4.661, P < 0.05; PD 28 vs PD 14, P = 0.025), but not in the BFD group (P > 0.05). Conclusions:,These studies reveal that the proportion of NMDA-EPSCs relative to glutamate-EPSCs and the decay time constant of NMDA-EPSCs are influenced by BFD. These changes may reflect important experience-dependent modifications of neuronal synapses in visual cortex. [source] CREATINE KINASE INHIBITOR IODOACETAMIDE ANTAGONIZES CALCIUM-STIMULATED INOTROPY IN CARDIOMYOCYTESCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2 2009Jun Ren SUMMARY 1Inhibition of creatine kinase is known to suppress cardiac contractile reserve in intact hearts, although the underlying mechanism has not been elucidated. 2The present study was designed to examine whether cardiac depression induced by creatine kinase inhibition was due to action at the level of the essential contractile element, namely cardiomyocytes. Adult rat cardiomyocytes were perfused with the creatine kinase inhibitor iodoacetamide (90 µmol/L) for 90 min. Mechanical and intracellular Ca2+ properties were evaluated using edge-detection and fluorescence microscopy, respectively. Myocytes were superfused with normal (1.3 mmol/L) or high (3.3 mmol/L) extracellular Ca2+ contractile buffer. Mechanical function was examined, including peak shortening (PS), maximal velocity of shortening/relengthening (±dL/dt), time to 90% PS (TPS90), time to 90% relengthening (TR90) and integration of shortening/relengthening (normalized to PS). Intracellular Ca2+ transients were evaluated using the following indices: resting and rise of fura-2 fluorescence intensity (,FFI) and intracellular Ca2+ decay time constant. 3The results indicate that elevated extracellular Ca2+ stimulated cardiomyocyte positive inotrope, manifested as increased PS, ±dL/dt, area of shortening, resting FFI and ,FFI associated with a shortened TR90 and intracellular Ca2+ decay time constant. High extracellular Ca2+ did not affect TPS90 and area of relengthening. Iodoacetamide ablated high Ca2+ -induced increases in PS, ±dL/dt, area of shortening, resting FFI, ,FFI and shortened TR90 and intracellular Ca2+ decay time constant. Iodoacetamide itself significantly enhanced the area of relengthening and TR90 without affecting other indices. 4Collectively, these data demonstrate that inhibition of creatine kinase blunts high extracellular Ca2+ -induced increases in cardiomyocyte contractile response (i.e. cardiac contractile reserve). [source] Electrical and neurotransmitter activity of mature neurons derived from mouse embryonic stem cells by Sox-1 lineage selection and directed differentiationEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2004R. J. Lang Abstract Sx1TV2/16C is a mouse embryonic stem (ES) cell line in which one copy of the Sox1 gene, an early neuroectodermal marker, has been targeted with a neomycin (G418) selection cassette. A combination of directed differentiation with retinoic acid and G418 selection results in an enriched neural stem cell population that can be further differentiated into neurons. After 6,7 days post-plating (D6,7PP) most neurons readily fired tetrodotoxin (TTX)-sensitive action potentials due to the expression of TTX-sensitive Na+ and tetraethylammonium (TEA)-sensitive K+ channels. Neurons reached their maximal cell capacitance after D6,7PP; however, ion channel expression continued until at least D21PP. The percentage of cells receiving spontaneous synaptic currents (s.s.c.) increased with days in culture until 100% of cells received a synaptic input by D20PP. Spontaneous synaptic currents were reduced in amplitude and frequency by TTX, or upon exposure to a Ca2+ -free, 2.5 mm Mg2+ saline. S.s.c. of rapid decay time constants were preferentially blocked by the nonNMDA glutamatergic receptor antagonists CNQX or NBQX. Ca2+ levels within ES cell-derived neurons increased in response to glutamate receptor agonists l -glutamate, AMPA, N -methyl- d -aspartate (NMDA) and kainic acid and to acetylcholine, ATP and dopamine. ES cell-derived neurons also generated cationic and Cl, -selective currents in response to NMDA and glycine or GABA, respectively. It was concluded that ES-derived neurons fire action potentials, receive excitatory and inhibitory synaptic input and respond to various neurotransmitters in a manner akin to primary central neurons. [source] Involvement of post-synaptic kainate receptors during synaptic transmission between unitary connections in rat neocortexEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2003Afia B. Ali Abstract The properties of functional kainate receptor-mediated EPSCs were studied in acute slices from 19,35-day-old rats. EPSCs elicited in pyramidal and fast-spiking cells in layers 2/3 and 5 of the rat motor cortex by extracellular single shock stimulus in the presence of GYKI 53655 and D-2-amino-5-phosphopentanoic resulted in a residual current. This current was not enhanced by cyclothiazide but was blocked by 6-cyano-7-nitroquinoxalin-2,3-dione and is thought to be mediated by kainate receptors. These kainate receptor-mediated currents displayed a wide range of time courses depending on which pre-synaptic fibres were activated. With paired recordings, unitary EPSCs elicited in pyramidal cells were almost totally blocked by GYKI 53655 and D-2-amino-5-phosphopentanoic. However, when L-transpyrrolidine-2,4-dicarboxylate (PDC), a glutamate uptake blocker, was introduced in the bath, the amplitude of kainate receptor-mediated currents, which is resistant to GYKI 53655 and D-2-amino-5-phosphopentanoic, was revealed. The rise and decay time constants of the kainate receptor-mediated currents were identical to control EPSCs. PDC was not required to reveal the kainate receptor-mediated currents elicited in fast-spiking cells which also displayed similar rise and decay time constants to the control EPSCs. Excitatory input onto pyramidal and fast-spiking cells in the neocortex mediated by kainate receptors contributed between 14 and 40% of the total control unitary EPSCs which displayed identical time courses to the AMPA receptor-mediated component of the EPSCs. Post-synaptic kainate receptors at connected pyramidal cell synapses may be located extra-synaptically. [source] Time-resolved spectroscopy in an undoped GaN (1-101)PHYSICA STATUS SOLIDI (C) - CURRENT TOPICS IN SOLID STATE PHYSICS, Issue 1 2008Eunhee Kim Abstract Time-resolved photoluminescence spectroscopy was performed at 77 K in a GaN (1-101) grown on a 7 degree off-axis (001) Si substrate. The sample was grown by metal-organic-vapour-phase-epitaxy (MOVPE) and was un-intentionally doped with O, C and Si. By using photoluminescence intensity correlation method, the energy relaxation process of the photogenerated carriers near the band edge was investigated in pico-second regime. The correlation signal was represented by a single exponential decay curve and the energy relaxation time was determined, which depended strongly on the kinetic energy of the excess carriers. At low energies, the relaxation time was around 700 ps, while it was as short as a few ps at the highest energy under study. The correlation signals obtained for carriers of which kinetic energy was less than 80 meV showed an anti-correlation behaviour suggesting the occurrence of carrier accumulation. The time constants for the accumulation were of several picoseconds depending on the kinetic energy, which was nearly equal to the decay time constants determined at high energies. This fact shows that the energy relaxation at high energies is controlled by the emission of an LO phonon. (© 2008 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] | |||||||||||||