Positive Voltage Range Research Articles

Can Anions Be Inserted into MXene?

Despite the continuous progress in the research and development of Ti3C2Tx (MXene) electrodes for high-power batteries and supercapacitor applications, the role of the anions in the electrochemical energy storage and their ability to intercalate between the MXene sheets upon application of positive voltage have not been clarified. A decade after the discovery of MXenes, the information about the possibility of anion insertion into the restacked MXene electrode is still being questioned. Since the positive potential stability range in diluted aqueous electrolytes is severely limited by anodic oxidation of the Ti, the possibility of anion insertion was evaluated in concentrated aqueous electrolyte solutions and aprotic electrolytes as well. To address this issue, we have conducted in situ gravimetric electrochemical quartz crystal microbalance with dissipation monitoring (EQCM-D) measurements in highly concentrated LiCl and LiBr electrolytes, which enable a significant extension of the operation range of the MXene electrodes toward positive potentials. Also, halogens are among the smallest anions and should be easier to intercalate between MXene layers, in comparison to multiatomic anions. On the basis of mass change variations in the positive voltage range and complementary density functional theory calculations, it was demonstrated that insertion of anionic species into MXene, within the range of potentials of interest for capacitive energy storage, is not likely to occur. This can be explained by the strong negative charge on Ti3C2Tx sheets terminated by functional groups.

Flexible Nonvolatile Bioresistive Random Access Memory with an Adjustable Memory Mode Capable of Realizing Logic Functions.

In this study, a flexible bioresistive memory with an aluminum/tussah hemolymph/indium tin oxide/polyethylene terephthalate structure is fabricated by using a natural biological material, tussah hemolymph (TH), as the active layer. When different compliance currents (Icc) are applied to the device, it exhibits different resistance characteristics. When 1 mA is applied in the positive voltage range and 100 mA is applied in the negative voltage range, the device exhibits bipolar resistive switching behavior. Additionally, when 1 mA is applied in both the positive- and negative-voltage ranges, the device exhibits write-once-read-many-times (WORM) characteristics. The device has good endurance, with a retention time exceeding 104 s. After 104 bending cycles, the electrical characteristics remain constant. This memory device can be applied for “AND” and “OR” logic operations in programmable logic circuits. The prepared flexible and transparent biomemristor made of pure natural TH provides a promising new approach for realizing environmentally friendly and biocompatible flexible memory, nerve synapses, and wearable electronic devices.

Structural transitions at electrodes, immersed in simple ionic liquid models.

We used a recently developed classical Density Functional Theory (DFT) method to study the structures, phase transitions, and electrochemical behaviours of two coarse-grained ionic fluid models, in the presence of a perfectly conducting model electrode. Common to both is that the charge of the cationic component is able to approach the electrode interface more closely than the anion charge. This means that the cations are specifically attracted to the electrode, due to surface polarization effects. Hence, for a positively charged electrode, there is competition at the surface between cations and anions, where the latter are attracted by the positive electrode charge. This generates demixing, for a range of positive voltages, where the two phases are structurally quite different. The surface charge density is also different between the two phases, even at the same potential. The DFT formulation contains an approximate treatment of ion correlations, and surface polarization, where the latter is modelled via screened image interactions. Using a mean-field DFT, where ion correlations are neglected, causes the phase transition to vanish for both models, but there is still a dramatic drop in the differential capacitance as proximal cations are replaced by anions, for increasing surface potentials. While these findings were obtained for relatively crude coarse-grained models, we argue that the findings can also be relevant in "real" systems, where we note that many ionic liquids are composed of a spherically symmetric anion, and a cation that is asymmetric both from a steric and a charge distribution point of view.

Polymeric phthalocyanine sheets as electrocatalytic electrodes for water-oxidation

Polymeric copper and cobalt phthalocyanine (Cu-pPc and Co-pPc) were prepared as thin films on fluorine-doped tin oxide (FTO) glass from evaporated metal films via a chemical vapor deposition (CVD) process with 1,2,4,5-tetracyanobenzene (TCB). The films were characterized by optical absorption spectroscopy in transmission and by X-ray photoelectron spectroscopy. Different oxidation states of the metal atoms were detected indicating different chemical environments. Reversible electrochemical reduction of Cu-pPc and Co-pPc was observed and monitored by cyclic voltammetry and spectroelectrochemical investigations. Cyclic voltammetry and chronoamperometry in the positive voltage range led to anodic currents in the oxygen evolution reaction that could be performed at stable current densities and showed a remarkable efficiency in particular for electrodes of Co-pPc in this reaction, attractive for the conversion of electrical energy into chemical energy.

Enhancement of an outwardly rectifying chloride channel in hippocampal pyramidal neurons after cerebral ischemia

Cerebral ischemia induces delayed, selective neuronal death in the CA1 region of the hippocampus. The underlying molecular mechanisms remain unclear, but it is known that apoptosis is involved in this process. Chloride efflux has been implicated in the progression of apoptosis in various cell types. Using both the inside-out and whole-cell configurations of the patch-clamp technique, the present study characterized an outwardly rectifying chloride channel (ORCC) in acutely dissociated pyramid neurons in the hippocampus of adult rats. The channel had a nonlinear current-voltage relationship with a conductance of 42.26±1.2pS in the positive voltage range and 18.23±0.96pS in the negative voltage range, indicating an outward rectification pattern. The channel is Cl− selective, and the open probability is voltage-dependent. It can be blocked by the classical Cl− channel blockers DIDS, SITS, NPPB and glibenclamide. We examined the different changes in ORCC activity in CA1 and CA3 pyramidal neurons at 6, 24 and 48h after transient forebrain ischemia. In the vulnerable CA1 neurons, ORCC activity was persistently enhanced after ischemic insult, whereas in the invulnerable CA3 neurons, no significant changes occurred. Further analysis of channel kinetics suggested that multiple openings are a major contributor to the increase in channel activity after ischemia. Pharmacological blockade of the ORCC partly attenuated cell death in the hippocampal neurons. We propose that the enhanced activity of ORCC might contribute to selective neuronal damage in the CA1 region after cerebral ischemia, and that ORCC may be a therapeutic target against ischemia-induced cell death.

Observation of negative differential resistance in GaN-based multiple-quantum-well light-emitting diodes

Anomalous current–voltage behaviors, such as negative differential resistance (NDR) and current hysteresis, are observed in the room-temperature current–voltage (I-V) curves of InGaN/GaN multiple-quantum-well light-emitting diodes. It is found that the NDR can be observed in the positive voltage range of the I-V curve only when the samples are pretreated with a negative voltage before sweeping, and the NDR disappears permanently after an over-current treatment. The dependence of the NDR upon the negative voltage and sweeping conditions leads to the conclusion that a variation of the charging state of the defect-induced hole traps is responsible for the anomalous I-V behaviors. Therefore, NDR is excluded as a feature of the tunneling transport mechanism, especially in GaN-based devices with a high defect density.

(Invited) A Metal Oxide Antifuse-Diode Device

Crystalline metal oxides have been used in various micro and nano electronics and optoelectronics, such as conductors, superconductors, and light emitting devices (LEDs). The amorphous metal oxide dielectric is usually a high-k material suitable for the insulation purpose. The doped metal oxide, such as the Zr-doped HfO2 (ZrHfO), high-k thin film has many advantageous material and electrical properties, such as the high crystallization temperature, low interface layer thickness in contact with Si, and low interface density of states (1). When nanocrystals are embedded into the high-k metal oxide dielectric thin film, electrons and charges can be stored for a long period of time, which is suitable for the nonvolatile memory application (2). Recently, it was proved by the author’s group that the broad band white light could be emitted from the metal oxide dielectric thin film after the dielectric breakdown due to the thermal excitation of the nano size conductive paths (3). In this talk, a new high-k dielectric based device that shows both antifuse and diode functions is reported. Figure 1 shows a large “programmed” to “unprogrammed” leakage current ratio of 105 is obtained from an original MOS capacitor made of a high-kgate dielectric on a p-type wafer, which fits the antifuse requirement. Figure 2 shows that for a same device in the programmed state, the leakage current increases with the increase of the magnitude of the gate voltage in the negative voltage range. However, the leakage current remains low and changes little over a large range of gate voltage in the positive voltage range, which is similar to the diode behavior. On the other hand, the leakage current-voltage curve of the new device is almost linear while that of the conventional diode follows the exponential relationship. The operation physics, structure, and material properties of the new device will be discussed in detail. Y. Kuo, J. Lu, S. Chatterjee, J. Yan, H. C. Kim, T. Yuan, W. Luo, J. Peterson, and M. Gardner, “Sub 2 nm Thick Zirconium Doped Hafnium Oxide High-K Gate Dielectrics,” ECS Trans., 1(5), 447-454 (2006).Y. Kuo, invited, “Nanocrystals Embedded High-k Nonvolatile Memories – bulk film and nanocrystal material effects,” ECS Trans., 53(4), 121-128 (2013).Y. Kuo, invited, “A Solid State Thin Film Incandescent Light Emitting Device,” Proc. IDEM, 104-107 (2014). Figure 1

Light Wavelength Effects on Charge Trapping and Detrapping of AlOx Embedded ZrHfO High-K Stack

The ZrHfO/AlOx/ZrHfO high-k gate dielectric memory capacitors on the p-type Si wafer have been fabricated using the one pumpdown sputtering process followed by rapid thermal annealing. The memory functions were mainly based on holes trapping at the AlOx site and AlOx/ZrHfO interface layer. The hole generation, transfer and storage in the dielectric structure was influenced by light exposure, e.g., the device retained fewer holes with the increase of the wavelength of the light. Under the light exposure, the leakage current decreased in the negative voltage range but increased in the large positive voltage range. The light exposure effect is important for practical applications of the device.

Fluorescently Labeled Tarantula Toxin Reveals Voltage Dependent Adhesion to K+ Channels

Among the most potent allosteric modulators of voltage-gated potassium channels are peptide toxins from arachnids. Guangxitoxin-1E is an exemplar of this class of ligands, having effects at nanomolar concentrations and shifting gating of Kv2.1 to a positive voltage range, beyond physiological potentials. We have synthesized biologically active variants of this toxin with unique chemically reactive groups that allow conjugation to probes that allow visualization of toxin adherence to channels on living cells. The association of toxin with Kv2.1 channels was found to be strongly voltage dependent, having different affinities for resting and activated states of voltage sensors. To compose structural hypotheses for the toxin-channel interactions that underlie allosteric effector properties, we built structural models of the toxin-channel interaction using the Rosetta-Membrane homology method and the Kv1.2-2.1 coordinates as template, to create models of Kv2.1 voltage sensing domains. Conformations of activated and resting states were generated following a sliding helix model. The toxin was then docked to these multiple voltage sensor conformations using the Rosetta Dock method to identify low energy complexes. Experimentally, measurement of toxin association and dissociation rates by voltage clamp and with fluorescently labeled toxins create constraints that define its mechanism of action. The differential adherence of toxin to resting and activated voltage sensor conformations drives allosteric modulation of channels. By measuring gating state-dependent affinities, this methodology creates a new means of assessing the potency and action of allosteric ion channel modulators. In combination with computational structure prediction and design this strategy could lead to development of voltage sensor modulators with novel state-dependence.

Zinc modulation of basal and β-adrenergically stimulated L-type Ca2+ current in rat ventricular cardiomyocytes: consequences in cardiac diseases

Zinc exists in biological systems as bound and histochemically reactive free Zn(2+) in the nanomolar range. Zinc is required as either structural or catalytic component for a large number of enzymes. It also modulates current passage through many ion channels. Here, we reinvestigated the effects of extracellular and intracellular Zn(2+) on the L-type Ca(2+) current (I (CaL)) and its modulation by β-adrenergic stimulation in rat ventricular cardiomyocytes. In the absence of Ca(2+) ions, Zn(2+) could permeate through the L-type channel at much lower concentrations and at a more positive voltage range, but with a lower permeability than Ca(2+). In the presence of Ca(2+), extracellular Zn(2+) demonstrated strong bimodal inhibitory effects on the I (CaL), with half-inhibition occurring around 30nM, i.e., in the range of concentrations found in the plasma. Intracellular Zn(2+) also significantly inhibited the I (CaL) with a half-inhibitory effect at 12.7nM. Moreover, β-adrenergic stimulation was markedly reduced by intracellular Zn(2+) at even lower concentrations (<1nM) as a consequence of Zn(2+)-induced inhibition of the adenylyl cyclase. All these effects appeared independent of redox variations and were not affected by dithiothreitol. Thus, both basal intracellular and extracellular Zn(2+) modulate transmembrane Ca(2+) movements and their regulation by β-adrenergic stimulation. Considering that, in many pathological situations, including diabetes, the extracellular Zn(2+) concentration is reduced and the intracellular one is increased, our results help to explain both Ca(2+) overload and marked reduction in the β-adrenergic stimulation in these diseases.

Light Wavelength Effects on Performance of a-Si:H PIN Photodiodes

ABSTRACTLight effects on the performance of the a-Si:H PIN photodiode has been studied. The leakage current-voltage and capacitance-voltage curves under the red, green and blue light illuminations were measured. The apparent charge storage density in the negative voltage range was quantified from the capacitance-voltage curve; charges in the positive voltage range were estimated from the leakage current-voltage curve. A comparison of charge storage capacities of diodes with different intrinsic layer thicknesses is also presented. The diode under the long wavelength light illumination condition stored more charges than that under the short wavelength light illumination condition because the former could penetrate the intrinsic a-Si:H layer deeper than the latter could. The leakage current and charge storage capacity of the diode are determined by the generation of electron-hole pairs, the depletion of charges in the intrinsic layer, and the supply of charges from the electrodes. The number of incident photons is critical to the process.

Extracellular Determinants of Anion Discrimination of the Cl−/H+ Antiporter Protein CLC-5

Mammalian CLC proteins comprise both Cl- channels and Cl-/H+ antiporters that carry out fundamental physiological tasks by transporting Cl- across plasma membrane and intracellular compartments. The NO3- over Cl- preference of a plant CLC transporter has been pinpointed to a conserved serine residue located at Scen and it is generally assumed that the other two binding sites of CLCs, Sext and Sin, do not substantially contribute to anion selectivity. Here we show for the Cl-/H+ antiporter CLC-5 that the conserved and extracellularly exposed Lys210 residue is critical to determine the anion specificity for transport activity. In particular, mutations that neutralize or invert the charge at this position reverse the NO3- over Cl- preference of WT CLC-5 at a concentration of 100 mm, but do not modify the coupling stoichiometry with H+. The importance of the electrical charge is shown by chemical modification of K210C with positively charged cysteine-reactive compounds that reintroduce the WT preference for Cl-. At saturating extracellular anion concentrations, neutralization of Lys210 is of little impact on the anion preference, suggesting an important role of Lys210 on the association rate of extracellular anions to Sext.

Voltage-Dependent Inactivation Gating at the Selectivity Filter of the MthK K+ channel

Voltage-dependent K+ channels can undergo a gating process known as C-type inactivation, which involves entry into a non-conducting state through conformational changes near the channel's selectivity filter. Here we report on a form of voltage-dependent inactivation gating observed in MthK, a prokaryotic Ca2+-gated K+ channel. In single-channel recordings, we observe that Po decreases with depolarization, with a half-maximal voltage of 96 ± 3 mV. This gating is kinetically distinct from blockade by internal Ca2+ or Ba2+, suggesting it may arise from an intrinsic inactivation mechanism. Inactivation gating was shifted toward more positive voltages by increasing external [K+] (47 mV per 10-fold increase in [K+]), suggesting that K+ binding at the extracellular side of the channel stabilizes the open-conductive state. The open-conductive state was stabilized by other external cations, and selectivity of the stabilizing site followed the sequence: K+ ≈ Rb+ > Cs+ > Na+ > Li+ ≈ NMG+. Selectivity of the stabilizing site is weaker than that of sites that determine permeability of these ions, suggesting that the site may lie toward the external end of the MthK selectivity filter. We could describe MthK gating over a wide range of positive voltages and external [K+] using kinetic schemes in which the open-conductive state is stabilized by K+ binding to a site that is not deep within the electric field, with the voltage-dependence of inactivation arising from both voltage-dependent K+ dissociation and transitions between non-conducting (inactivated) states. These results provide a quantitative working hypothesis for voltage-dependent, K+-sensitive inactivation gating, a property that may be common to other K+ channels.

Voltage-dependent inactivation gating at the selectivity filter of the MthK K+ channel

Voltage-dependent K+ channels can undergo a gating process known as C-type inactivation, which involves entry into a nonconducting state through conformational changes near the channel’s selectivity filter. C-type inactivation may involve movements of transmembrane voltage sensor domains, although the mechanisms underlying this form of inactivation may be heterogeneous and are often unclear. Here, we report on a form of voltage-dependent inactivation gating observed in MthK, a prokaryotic K+ channel that lacks a canonical voltage sensor and may thus provide a reduced system to inform on mechanism. In single-channel recordings, we observe that Po decreases with depolarization, with a half-maximal voltage of 96 ± 3 mV. This gating is kinetically distinct from blockade by internal Ca2+ or Ba2+, suggesting that it may arise from an intrinsic inactivation mechanism. Inactivation gating was shifted toward more positive voltages by increasing external [K+] (47 mV per 10-fold increase in [K+]), suggesting that K+ binding at the extracellular side of the channel stabilizes the open-conductive state. The open-conductive state was stabilized by other external cations, and selectivity of the stabilizing site followed the sequence: K+ ≈ Rb+ > Cs+ > Na+ > Li+ ≈ NMG+. Selectivity of the stabilizing site is weaker than that of sites that determine permeability of these ions, suggesting that the site may lie toward the external end of the MthK selectivity filter. We could describe MthK gating over a wide range of positive voltages and external [K+] using kinetic schemes in which the open-conductive state is stabilized by K+ binding to a site that is not deep within the electric field, with the voltage dependence of inactivation arising from both voltage-dependent K+ dissociation and transitions between nonconducting (inactivated) states. These results provide a quantitative working hypothesis for voltage-dependent, K+-sensitive inactivation gating, a property that may be common to other K+ channels.

Structural Modifications to Convert Melittin from a Cytolytic Peptide to a Stable Cargo Linker

Melittin is a 26 amino acid peptide that comprises more than half of the dry weight of the venom of the honeybee Apis Mellifera. In previous studies, we demonstrated that melittin stably bound to the lipid membrane of perfluorocarbon (PFC) nanoparticles and served as an active anti-cancer therapeutic agent in vivo (Soman et al. J Clin Invest. 2009). Here, we report the structure modification that converts the mellittin to a cargo linker for post-formulation liposome customization. We introduced point mutations and truncations to define the lytic and membrane binding activities of melittin. For each of the mutations, lytic activity of the peptides was tested by the carboxyfluorescein fluorescence dequenching assay on carboxyfluorescein encapsulated liposomes. Among all six melittin mutations, the mutation, D1-7, with the first 7 amino acids removed (VLTTGLPALISWIKRKRQQ) dramatically reduces the melittin lytic activity. Using immobilized Giant Unilamellar Vesicles (GUV), we illustrated that at peptide:lipid ratio of 40:1, D1-7 bound to the GUV without pore forming, while at peptide:lipid ratio of 1:83, melittin already formed pores on the GUV membrane. These results suggest that D1-7 eliminates the lytic activity but retains the strong lipid membrane binding. For further confirmation, we measured liposome sizes and zeta potentials with and without D1-7 loading. Consistently, D1-7 did not affect the size of the liposome, but shifted the zeta potential (or surface charge) of the liposome towards the positive voltage range, because D1-7 is a positively charged peptide. Among numerous existing nanosystems for drug delivery, liposomes are approved by FDA for anti-cancer and gene therapy. Accordingly, this linker and/or its refinements could enhance the therapeutic potential of approved liposomal drugs by enabling flexible incorporation and cargo multiplexing through post-formulation surface editing.

Cardiac Ion Channels

The analysis of the molecular basis of the inherited cardiac arrhythmias has been the driving force behind the identification of the ion channels that generate the action potential. The genes encoding all the major ion channels have cloned and sequenced. The studies have revealed greater complexity than heretofore imagined. Many ion channels function as part of macromolecular complexes in which many components are assembled at specific sites within the membrane. This review describes the generation of the normal cardiac action potential. The properties of the major ionic currents are the examined in detail. Special emphasis is placed on the functional consequences of arrhythmia-associated ion channel mutations. The review concludes with a glimpse of the directions in which this new electrophysiology may lead. The normal sequence and synchronous contraction of the atria and ventricles require the rapid activation of groups of cardiac cells. An activation mechanism must enable rapid changes in heart rate and also respond to the changes in autonomic tone. The propagating cardiac action potential fulfils these roles. Figure 1 illustrates the 5 phases of the normal action potential: 1. Phase 4, or the resting potential, is stable at ≈−90 mV in normal working myocardial cells. 2. Phase 0 is the phase of rapid depolarization. The membrane potential shifts into positive voltage range. This phase is central to rapid propagation of the cardiac impulse (conduction velocity, θ=1 m/s). 3. Phase 1 is a phase of rapid repolarization. This phase sets the potential for the next phase of the action potential. 4. Phase 2, a plateau phase, is the longest phase. It is unique among excitable cells and marks the phase of calcium entry into the cell. 5. Phase 3 is the phase of rapid repolarization that restores the membrane potential to its resting value.1 Figure 1. Membrane currents that generate the a normal …

Conversion of the 2 Cl−/1 H+ antiporter ClC-5 in a NO3−/H+ antiporter by a single point mutation

Several members of the CLC family are secondary active anion/proton exchangers, and not passive chloride channels. Among the exchangers, the endosomal ClC-5 protein that is mutated in Dent's disease shows an extreme outward rectification that precludes a precise determination of its transport stoichiometry from measurements of the reversal potential. We developed a novel imaging method to determine the absolute proton flux in Xenopus oocytes from the extracellular proton gradient. We determined a transport stoichiometry of 2 Cl(-)/1 H+. Nitrate uncoupled proton transport but mutating the highly conserved serine 168 to proline, as found in the plant NO3(-)/H+ antiporter atClCa, led to coupled NO3(-)/H+ exchange. Among several amino acids tested at position 168, S168P was unique in mediating highly coupled NO3(-)/H+ exchange. We further found that ClC-5 is strongly stimulated by intracellular protons in an allosteric manner with an apparent pK of approximately 7.2. A 2:1 stoichiometry appears to be a general property of CLC anion/proton exchangers. Serine 168 has an important function in determining anionic specificity of the exchange mechanism.

An Outwardly Rectifying Chloride Channel in Human Atrial Cardiomyocytes

Among a range of chloride channels, outwardly rectifying Cl- channels have been reported in the heart of various species. Although the anionic current carried by this channel has been subjected to intense electrophysiological investigations, paradoxically no examination of single-channel currents has been reported for human cardiomyocytes. Using the cell-attached and cell-free configurations of the patch-clamp technique, we have characterized the properties of an outwardly rectifying chloride current (ORCC) at the unitary level in freshly isolated human atrial cardiomyocytes. In excised inside-out patches, the channel presented a nonlinear I/V relationship with a conductance of 76.5 +/- 14.7 pS in the positive voltage range and 8.1 +/- 2 pS in the negative voltage range, indicating an outward rectification. Preincubation with the protein kinase C activator phorbol 12-myristate 13-acetate (PMA) significantly increased the number of spontaneously active channels observed. The channel was Cl- selective (Cl- to Na+ permeability ratio, PCl/PNa= 18) with the permeability sequence I- > Br- > Cl- > F- > gluconate. It was blocked by the classical Cl- channels blockers glibenclamide, NPPB, SITS, and DIDS. Channel activity was not dependent upon internal calcium concentration. In the cell-attached configuration, ORCC channel activation was observed under perfusion of a hypotonic solution. Human atrial myocytes express an outwardly rectifying Cl- channel that is sensitive to PKC activation. This channel shares biophysical and pharmacological properties with the swelling-activated chloride current implicated in cardiac pathologies such as myocardial ischemia and dilated cardiopathies.

Gating of TRP channels: a voltage connection?

TRP channels represent the main pathways for cation influx in non-excitable cells. Although TRP channels were for a long time considered to be voltage independent, several TRP channels now appear to be weakly voltage dependent with an activation curve extending mainly into the non-physiological positive voltage range. In connection with this voltage dependence, there is now abundant evidence that physical stimuli, such as temperature (TRPV1, TRPM8, TRPV3), or the binding of various ligands (TRPV1, TRPV3, TRPM8, TRPM4), shift this voltage dependence towards physiologically relevant potentials, a mechanism that may represent the main functional hallmark of these TRP channels. This review discusses some features of voltage-dependent gating of TRPV1, TRPM4 and TRPM8. A thermodynamic principle is elaborated, which predicts that the small gating charge of TRP channels is a crucial factor for the large voltage shifts induced by various stimuli. Some structural considerations will be given indicating that, although the voltage sensor is not yet known, the C-terminus may substantially change the voltage dependence of these channels.

TRP channels: novel gating properties and physiological functions

TRP channels: novel gating properties and physiological functions