Dependent Rectification Research Articles

Voltage and frequency controlled Ge/SeO2 thin film transistors designed as rectifiers, negative capacitance and negative conductance sources

Herein voltage and frequency controlled thin film transistors fabricated by depositing SeO2 onto germanium thin crystals are reported. For these devices measurements of the current-voltage characteristics revealed a biasing dependent rectification ratios. The devices showed metal-oxide-semiconductor character under reverse biasing conditions. In addition, the biasing dependent capacitance and conductance spectral studies in the frequency domain of 20M-1000MHz has shown the possibility of switching the capacitance and negative conductance from negative mode to positive mode. The features of the Ge/SeO2 devices make them attractive for use in electronic circuits as parasitic capacitive circuit elements, noise reducers, signal amplifiers and microwave oscillators.

Impact of ISK Voltage and Ca2+/Mg2+-Dependent Rectification on Cardiac Repolarization

Cardiac small conductance Ca2+-activated K+ (SK) channels are activated solely by Ca2+, but the SK current (ISK) is inwardly rectified. However, the impact of inward rectification in shaping action potentials (APs) in ventricular cardiomyocytes under β-adrenergic stimulation or in disease states remains undefined. Two processes underlie this inward rectification: an intrinsic rectification caused by an electrostatic energy barrier from positively charged amino acids at the inner pore and a voltage-dependent Ca2+/Mg2+ block. Thus, Ca2+ has a biphasic effect on ISK, activating at low [Ca2+] yet inhibiting ISK at high [Ca2+]. We examined the effect of ISK rectification on APs in rat cardiomyocytes by simultaneously recording whole-cell apamin-sensitive currents and Ca2+ transients during an AP waveform and developed a computer model of SK channels with rectification features. The typical profile of ISK during AP clamp included an initial peak (mean 1.6 pA/pF) followed by decay to the point that submembrane [Ca2+] reached ∼10 μM. During the rest of the AP stimulus, ISK either plateaued or gradually increased as the cell repolarized and submembrane [Ca2+] decreased further. We used a six-state gating model combined with intrinsic and Ca2+/Mg2+-dependent rectification to simulate ISK and investigated the relative contributions of each type of rectification to AP shape. This SK channel model replicates key features of ISK recording during AP clamp showing that intrinsic rectification limits ISK at high Vm during the early and plateau phase of APs. Furthermore, the initial rise of Ca2+ transients activates, but higher [Ca2+] blocks SK channels, yielding a transient outward-like ISK trajectory. During the decay phase of Ca2+, the Ca2+-dependent block is released, causing ISK to rise again and contribute to repolarization. Therefore, ISK is an important repolarizing current, and the rectification characteristics of an SK channel determine its impact on early, plateau, and repolarization phases of APs.

The Aromatic Thermosetting Copolyester for Schottky Diode Applications in a Wide Temperature Range

The aromatic thermosetting copolyester (ATSP) was deposited on p-Si substrates by the spin coating method, and the thickness of thin film layer was about 50 nm. It was employed to fabricate metal-polymer-semiconductor (MPS) heterojunctions as interfacial layers between metal contact and p type Si. The morphological properties of the Al/ATSP/p-Si heterojunctions were investigated by Scanning Electron Microscope (SEM) and an Atomic Force Microscope. The electrical characteristics of the heterojunctions were analyzed within a wide temperature range between 100 K and 500 K and frequency range. The current–voltage–temperature (I–V–T) characteristics of the MPS heterojunctions were explained by the Thermionic Emission (TE) theory and Norde function. Critical electrical parameters including leakage current (I0), barrier height (Φb) and ideality factor (n) and series resistance (Rs) were calculated by I–V–T characteristics in dark conditions. The value of n and Φb was obtained as 2.56 and 0.78 eV at 300 K. The n and Φb values were obtained as strong function of the temperature depending on barrier inhomogeneity. The temperature dependent rectification ratios of the Al/ATSP/p-Si heterojunctions were calculated and discussed in the details considering effective operating temperatures. The capacitance–voltage (C–V) and conductance–voltage (G–V) characteristics were measured at 300 K. To obtain Fermi energy (EF), donor concentration (Na), maximum electric field (Em), Φb and interface states (Nss), were performed on the bases of voltage and frequency at 300 K. From the electrical analysis results, it is proposed that the MPS device can be employed in electronic devices at low and high temperatures.

The Role of PLCδ4 in the Activity of TRPM8 Expressing Sensory Neurons

Changes in environmental temperature are sensed by the peripheral endings of dorsal root ganglion (DRG) neurons. A subset of neurons expressing Transient Receptor Potential Melastatin 8 (TRPM8) channels function as major sensors of moderately cold temperatures. Previously it was demonstrated that Ca2+ influx through recombinant TRPM8 activates a Ca2+ sensitive phospholipase C (PLC) isoform, leading to depletion of phosphatidylinositol 4,5-bisphosphate with subsequent decrease of the TRPM8 currents (desensitization). We have found earlier that the most abundant highly Ca2+ sensitive PLC isoform in DRG neurons is PLCδ4. We performed patch-clamp experiments on TRPM8 expressing DRG neurons from PLCδ4-KO and WT animals, and identified 2 neuronal subpopulations based of their size. Small neurons had significantly larger TRPM8 current densities compared to the medium-large ones. PLCδ4-KO cells had larger currents upon menthol application and diminished desensitization. Current-clamp experiments further confirmed the differences in these subgroups. Both KO and WT small neurons had a more depolarized resting membrane potential than medium-large cells, and required smaller current injection to generate action potentials (AP) indicating their higher excitability. Positive current injection initially induced a train of AP during current pulses; increasing the current magnitude lead to a profound decline of the AP frequency in WT but KO neurons were able to generate AP at maximal frequency. AP shape and characteristics were also different for small and medium-large neurons. Negative current injection demonstrated characteristic voltage- and time- dependent rectification and rebound spike for both WT and KO small neurons. Menthol application induced transient generation of AP with frequency significantly higher in KO and larger depolarization compare to the WT neurons. Our present data support the role of PLCδ4 in the process of TRPM8 desensitization.

Magnetization dependent rectification in (Ga,Mn)As tri-layer tunnel junctions

Current rectification in (Ga,Mn)As tri-layer magnetic tunnel junctions (MTJs) is found to be controllable through the alignment of magnetizations, which can be changed with small current injections. The tunneling magnetoresistance (TMR) at 4.2K is 120% in amplitude, showing three step structure, which corresponds to the alignment of magnetizations. With a minor field loop, the alignment of magnetization can be anti-parallel for the top and the bottom layers and then current injections with alternative direction can reverse the direction of the magnetization in the middle layer. The threshold current is as low as 2 × 104A/cm2. We have found the junctions have small rectification effect up to 8GHz, which is strongly dependent on the alignment of the magnetization. Hence the direction of the rectification as well as the amplitude can be switched by the bi-directional current injections. The rectification can be explained within the Julliere model with enegy dependence of the density of states. To check this we performed tunneling measurements and obtained positive results.

Permeation properties of the hair cell mechanotransducer channel provide insight into its molecular structure

Mechanoelectric transducer (MET) channels, located near stereocilia tips, are opened by deflecting the hair bundle of sensory hair cells. Defects in this process result in deafness. Despite this critical function, the molecular identity of MET channels remains a mystery. Inherent channel properties, particularly those associated with permeation, provide the backbone for the molecular identification of ion channels. Here, a novel channel rectification mechanism is identified, resulting in a reduced pore size at positive potentials. The apparent difference in pore dimensions results from Ca(2+) binding within the pore, occluding permeation. Driving force for permeation at hyperpolarized potentials is increased because Ca(2+) can more easily be removed from binding within the pore due to the presence of an electronegative external vestibule that dehydrates and concentrates permeating ions. Alterations in Ca(2+) binding may underlie tonotopic and Ca(2+)-dependent variations in channel conductance. This Ca(2+)-dependent rectification provides targets for identifying the molecular components of the MET channel.

Family-Dependent Rectification Characteristics in Ultra-Short Graphene Nanoribbon p–n Junctions

We present the first transport property investigation of a-few-nanometer-long armchair graphene nanoribbon (AGNR) p–n junctions by using first-principles method. Intriguingly, family dependent rectification is observed. To be specific, traditional rectification effect in the forward direction is observed in the AGNR p–n junctions with 3n and 3n + 2 widths, whereas reverse rectification effect is observed in the AGNR p–n junctions with 3n + 1 width. The analysis of the spatial distribution of molecular projected self-consistent Hamiltonian eigenstates and the projected density of states give an insight into the observed results.

Inactivation and Voltage-Dependent Rectification Mechanisms in the KcsA Potassium Channel

Potassium channels regulate ion permeation by varying their conductance notably through a mechanism known as C-type inactivation, which implies that shortly after activation, their selectivity filter stops conducting ions at rates that depend on various stimuli. This inactivation process plays a critical role in controlling the length and frequency of cardiac action potentials, as well as the firing patterns in neurons.It's been shown that the prokaryotic KcsA channel undergoes C-type inactivation like its eukaryotic counterparts (Gao et al., PNAS 102:17630 (2005)), suggesting KcsA as a prototypic model for structural studies of inactivation gating. The detailed microscopic process underlying C-type inactivation remains unexplained despite the accumulation of experimental evidences showing the key role played by the selectivity filter and some neighboring residues. In particular, the interactions between Asp80, Glu71 and Trp67, as well as the water molecules trapped in the P-loop of the channel, seem to be strongly linked to the stability of the filter and its ability to adopt a stable inactivated state (Cordero-Morales et al., Nat. Struct. & Mol. Biol. 14:1062 (2007)). Models of inactivation gating that were proposed on the basis of x-ray crystallography studies involve transitions between conducting states, containing two ions, and non conducting ones, containing a single ion (Zhou et al., Nature 414:23 (2001); Cuello et al., Nature 466:272 (2010)).Using molecular dynamic simulations and free energy calculations, we investigated the possible transitions between different ion occupancy states involving the conducting and putatively inactivated conformations of KcsA. A comparative study of key mutants showing different inactivation phenotypes allows us to propose a structural model describing the inactivation mechanism of KcsA, as well as the voltage dependent rectification observed in WT and some mutants.

TMEM16B induces chloride currents activated by calcium in mammalian cells

Ca(2+)-activated Cl(-) channels play important physiological roles in various cell types, but their molecular identity is still unclear. Recently, members of the protein family named transmembrane 16 (TMEM16) have been suggested to function as Ca(2+)-activated Cl(-) channels. Here, we report the functional properties of mouse TMEM16B (mTMEM16B) expressed in human embryonic kidney (HEK) 293T cells, measured both in the whole-cell configuration and in inside-out excised patches. In whole cell, a current induced by mTMEM16B was activated by intracellular Ca(2+) diffusing from the patch pipette, released from intracellular stores through activation of a G-protein-coupled receptor, or photoreleased from caged Ca(2+) inside the cell. In inside-out membrane patches, a current was rapidly activated by bath application of controlled Ca(2+) concentrations, indicating that mTMEM16B is directly gated by Ca(2+). Both in the whole-cell and in the inside-out configurations, the Ca(2+)-induced current was anion selective, blocked by the Cl(-) channel blocker niflumic acid, and displayed a Ca(2+)-dependent rectification. In inside-out patches, Ca(2+) concentration for half-maximal current activation decreased from 4.9 microM at -50 mV to 3.3 microM at +50 mV, while the Hill coefficient was >2. In inside-out patches, currents showed a reversible current decrease at -50 mV in the presence of a constant high Ca(2+) concentration and, moreover, an irreversible rundown, not observed in whole-cell recordings, indicating that some unknown modulator was lost upon patch excision. Our results demonstrate that mTMEM16B functions as a Ca(2+)-activated Cl(-) channel when expressed in HEK 293T cells.

Pentobarbital depressant effects are independent of GABA receptors in auditory thalamic neurons.

Pentobarbital, a general anesthetic, has received extensive study for its ability to potentiate inhibition at GABA(A) subtype of receptors for GABA. Using whole cell current-clamp techniques and bath applications, we determined the effects of pentobarbital and GABA receptor antagonists on the membrane properties and tonic or burst firing of medial geniculate neurons in thalamic slices. Pentobarbital (0.01-200 microM) induced depressant effects in 50 of 66 neurons (76%). Pentobarbital hyperpolarized neurons by a mean of 3 mV and decreased the number of action potentials in tonic firing, evoked by current pulse injection from near the resting potential. Pentobarbital also decreased burst firing or low threshold Ca(2+)-spikes, evoked by current pulse injection into neurons at potentials hyperpolarized from rest. The blockade of tonic and burst firing, as well as low threshold Ca(2+)-spikes, was surmountable by increasing the amplitude of input current. The GABA(A) receptor antagonists, bicuculline (100 microM) and picrotoxinin (50-100 microM), did not block the depressant effects of pentobarbital (10 microM). The GABA(B) receptor antagonist, saclofen (200 microM), and GABA(C) receptor antagonist, (1,2,3,6-tetrahydropyridine-4-yl)methylphosphinate (10-50 microM), did not significantly alter the depressant effects. Pentobarbital produced excitatory effects (0.1-50 microM) on 11 neurons (17%) but had no effects on 5 neurons (7%). The excitation consisted of approximately 3 mV depolarization, increased tonic and burst firing and the rate of rise and amplitude of low threshold Ca(2+) spikes. These effects were associated with a increase in input resistance. In contrast, the depressant effects of pentobarbital correlated to a decreased input resistance measured with hyperpolarizing current pulse injection (IC(50) = 7.8 microM). Pentobarbital reduced Na(+)-dependent rectification on depolarization and lowered the slope resistance over a wide voltage range. Tetrodotoxin eliminated both Na(+)-dependent rectification and the pentobarbital-induced decrease in membrane resistance at depolarized voltages in two-thirds of the neurons. The pentobarbital-induced decrease in membrane resistance at voltages hyperpolarized from rest was not evident during co-application with Cs(+), known to block the hyperpolarization-activated rectifiers. In summary, the pentobarbital acted at low concentrations to depress thalamocortical neurons. The depression resulted from decreased rectification on depolarization, which no longer boosted potentials over threshold, and an increased conductance that shunted spike generation. The depressant effects of pentobarbital did not involve known types of GABA receptor interactions.

Molecular Determinants of Permeation through the Cation Channel TRPV4

We have studied the molecular determinants of ion permeation through the TRPV4 channel (VRL-2, TRP12, VR-OAC, and OTRPC4). TRPV4 is characterized by both inward and outward rectification, voltage-dependent block by Ruthenium Red, a moderate selectivity for divalent versus monovalent cations, and an Eisenman IV permeability sequence. We identify two aspartate residues, Asp(672) and Asp(682), as important determinants of the Ca(2+) sensitivity of the TRPV4 pore. Neutralization of either aspartate to alanine caused a moderate reduction of the relative permeability for divalent cations and of the degree of outward rectification. Neutralizing both aspartates simultaneously caused a much stronger reduction of Ca(2+) permeability and channel rectification and additionally altered the permeability order for monovalent cations toward Eisenman sequence II or I. Moreover, neutralizing Asp(682) but not Asp(672) strongly reduces the affinity of the channel for Ruthenium Red. Mutations to Met(680), which is located at the center of a putative selectivity filter, strongly reduced whole cell current amplitude and impaired Ca(2+) permeation. In contrast, neutralizing the only positively charged residue in the putative pore region, Lys(675), had no obvious effects on the properties of the TRPV4 channel pore. Our findings delineate the pore region of TRPV4 and give a first insight into the possible architecture of its permeation pathway.

Anion Channels in Chara corallina Tonoplast Membrane: Calcium Dependence and Rectification

Tonoplast K(+) channels of Chara corallina are well characterized but only a few reports mention anion channels, which are likely to play an important role in the tonoplast action potential and osmoregulation of this plant. For experiments internodal cells were isolated. Cytoplasmic droplets were formed in an iso-osmotic bath solution according to a modified procedure. Ion channels with conductances of 48 pS and 170 pS were detected by the patch-clamp technique. In the absence of K(+) in the bath solution the 170 pS channel was not observed at negative pipette potential values. When Cl(-) on either the vacuolar side or the cytoplasmic side was partly replaced with F(-), the reversal potential of the 48 pS channel shifted conform to the Cl(-) equilibrium potential with similar behavior in droplet-attached and excised patch mode. These results showed that the 48 pS channel was a Cl(-) channel. In droplet-attached mode the channel rectified outward current flow, and the slope conductance was smaller. When Chara droplets were formed in a bath solution containing low (10(-8) m) Ca(2+), then no Cl(-) channels could be detected either in droplet-attached or in inside-out patch mode. Channel activity was restored if Ca(2+) was applied to the cytoplasmic side of inside-out patches. Rectification properties in the inside-out patch configuration could be controlled by the holding pipette potential. Holding potential values negative or positive to the calculated reversal potential for Cl(-) ions induced opposite rectification properties. Our results show Ca(2+)-activated Cl(-) channels in the tonoplast of Chara with holding potential dependent rectification.