Here we report a fully flexible, foldable nanopatterned wearable triboelectric nanogenerator (WTNG) with high power-generating performance and mechanical robustness. Both a silver (Ag)-coated textile and polydimethylsiloxane (PDMS) nanopatterns based on ZnO nanorod arrays on a Ag-coated textile template were used as active triboelectric materials. A high output voltage and current of about 120 V and 65 μA, respectively, were observed from a nanopatterned PDMS-based WTNG, while an output voltage and current of 30 V and 20 μA were obtained by the non-nanopatterned flat PDMS-based WTNG under the same compressive force of 10 kgf. Furthermore, very high voltage and current outputs with an average value of 170 V and 120 μA, respectively, were obtained from a four-layer-stacked WTNG under the same compressive force. Notably it was found there are no significant differences in the output voltages measured from the multilayer-stacked WTNG over 12 000 cycles, confirming the excellent mechanical durability of WTNGs. Finally, we successfully demonstrated the self-powered operation of light-emitting diodes, a liquid crystal display, and a keyless vehicle entry system only with the output power of our WTNG without any help of external power sources.

Auditory fear memory is thought to be maintained by fear conditioning-induced potentiation of synaptic efficacy, which involves enhanced expression of surface AMPA receptor (AMPAR) at excitatory synapses in the lateral amygdala (LA). Depotentiation, reversal of conditioning-induced potentiation, has been proposed as a cellular mechanism for fear extinction; however, a direct link between depotentiation and extinction has not yet been tested. To address this issue, we applied both ex vivo and in vivo approaches to rats in which fear memory had been consolidated. A unique form of depotentiation reversed conditioning-induced potentiation at thalamic input synapses onto the LA (T-LA synapses) ex vivo. Extinction returned the enhanced T-LA synaptic efficacy observed in conditioned rats to baseline and occluded the depotentiation. Consistently, extinction reversed conditioning-induced enhancement of surface expression of AMPAR subunits in LA synaptosomal preparations. A GluR2-derived peptide that blocks regulated AMPAR endocytosis inhibited depotentiation, and microinjection of a cell-permeable form of the peptide into the LA attenuated extinction. Our results are consistent with the use of depotentiation to weaken potentiated synaptic inputs onto the LA during extinction and provide strong evidence that AMPAR removal at excitatory synapses in the LA underlies extinction.lateral amygdala ͉ fear conditioning ͉ AMPA receptor ͉ endocytosis T he cortical and thalamic input synapses onto the lateral amygdala (LA) (C-LA and T-LA synapses, respectively) carry auditory information from the auditory cortex and auditory thalamus onto the LA, respectively (1). Long-term potentiation (LTP; an in vitro model of memory) (2)-like changes in these pathways are thought to underlie both the encoding and consolidation of auditory fear memory (3-8). The results of a recent study suggest that long-term retention of conditioning-induced potentiation at excitatory synapses in the LA is a critical requirement for consolidated fear memory within the LA (7, 9). Also, LTP requiring the synaptic delivery of AMPA receptors (AMPARs) at excitatory synapses in the LA appears to be necessary for establishing consolidated fear memory (6,8,10). Conditioning-induced potentiation and auditory fear memory encoded in the LA have been shown to be consolidated within 24 h after fear conditioning (5, 7, 11). Moreover, auditory fear memory appears to be maintained in the LA across the adult lifetime of rats (12). Thus, consolidation of auditory fear memory encoded in the LA is rapid and localized, unlike hippocampus-dependent memory, which involves slow and distributed consolidation processes (13).In the present study, we tested the hypothesis that depotentiation of conditioning-induced potentiation at excitatory synapses in the LA underlies extinction of consolidated fear memory. Synaptic weights were monitored ex vivo by using whole-cell (or field potential) recordings in amygdala slices prepared from behaviortrained rats. Results Extinction of Consolidated ...

Transparent flexible graphene triboelectric nanogenerators as new promising applications of chemical vapor deposition‐grown graphene are successfully demonstrated. The work function and friction are decisive factors to understand the difference in output performance depending on the number of layers of graphene. In this work, we were able to power an LCD, LEDs, and an EL display using the electrical power output of the graphene triboelectric nanogenerator without any external energy source.

Hydrophobic sponge structure-based triboelectric nanogenerators using an inverse opal structured film for sustainable energy harvesting over a wide range of humid atmosphere have been successfully demonstrated. The output voltage and current density reach a record value of 130 V and 0.10 mA cm(-2) , respectively, giving over 10-fold power enhancement, compared with the flat film-based triboelectric nanogenerator.

Hyperpolarization-activated cation currents (Ih) are key determinants of repetitive electrical activity in heart and nerve cells. The bradycardic agent ZD7288 is a selective blocker of these currents. We studied the mechanism for ZD7288 blockade of cloned Ih channels in excised inside-out patches. ZD7288 blockade of the mammalian mHCN1 channel appeared to require opening of the channel, but strong hyperpolarization disfavored blockade. The steepness of this voltage-dependent effect (an apparent valence of ∼4) makes it unlikely to arise solely from a direct effect of voltage on blocker binding. Instead, it probably indicates a differential affinity of the blocker for different channel conformations. Similar properties were seen for ZD7288 blockade of the sea urchin homologue of Ih channels (SPIH), but some of the blockade was irreversible. To explore the molecular basis for the difference in reversibility, we constructed chimeric channels from mHCN1 and SPIH and localized the structural determinant for the reversibility to three residues in the S6 region likely to line the pore. Using a triple point mutant in S6, we also revealed the trapping of ZD7288 by the closing of the channel. Overall, the observations led us to hypothesize that the residues responsible for ZD7288 block of Ih channels are located in the pore lining, and are guarded by an intracellular activation gate of the channel.

Voltage-activated K+ channels are integral membrane proteins containing a potassium-selective transmembrane pore gated by changes in the membrane potential. This activation gating (opening) occurs in milliseconds and involves a gate at the cytoplasmic side of the pore. We found that substituting cysteine at a particular position in the last transmembrane region (S6) of the homotetrameric Shaker K+ channel creates metal binding sites at which Cd2+ ions can bind with high affinity. The bound Cd2+ ions form a bridge between the introduced cysteine in one channel subunit and a native histidine in another subunit, and the bridge traps the gate in the open state. These results suggest that gating involves a rearrangement of the intersubunit contacts at the intracellular end of S6. The recently solved structure of a bacterial K+ channel shows that the S6 homologs cross in a bundle, leaving an aperture at the bundle crossing. In the context of this structure, the metal ions form a bridge between a cysteine above the bundle crossing and a histidine below the bundle crossing in a neighboring subunit. Our results suggest that gating occurs at the bundle crossing, possibly through a change in the conformation of the bundle itself.

Hyperpolarization-activated HCN channels are modulated by direct binding of cyclic nucleotides. For HCN2 channels, cAMP shifts the voltage dependence for activation, with relatively little change in the maximal conductance. By contrast, in spHCN channels, cAMP relieves a rapid inactivation process and produces a large increase in maximum conductance. Our results suggest that these two effects of cAMP represent the same underlying process. We also find that spHCN inactivation occurs not by closure of a specialized inactivation gate, as for other voltage-dependent channels, but by reclosure of the same intracellular gate opened upon activation. Effectively, the activation gate exhibits a "desensitization to voltage," perhaps by slippage of the coupling between the voltage sensors and the gate. Differences in the initial coupling efficiency could allow cAMP to produce either the inactivation or the shift phenotype by strengthening effective coupling: a shift would naturally occur if coupling is already strong in the absence of cAMP.

Hyperpolarization-activated cation (HCN) channels regulate pacemaking activity in cardiac cells and neurons. Our previous work using the specific HCN channel blocker ZD7288 provided evidence for an intracellular activation gate for these channels because it appears that ZD7288, applied from the intracellular side, can enter and leave HCN channels only at voltages where the activation gate is opened (Shin, K.S., B.S. Rothberg, and G. Yellen. 2001. J. Gen. Physiol. 117:91–101). However, the ZD7288 molecule is larger than the Na+ or K+ ions that flow through the open channel. In the present study, we sought to resolve whether the voltage gate at the intracellular entrance to the pore for ZD7288 also can be a gate for permeant ions in HCN channels. Single residues in the putative pore-lining S6 region of an HCN channel (cloned from sea urchin; spHCN) were substituted with cysteines, and the mutants were probed with Cd2+ applied to the intracellular side of the channel. One mutant, T464C, displayed rapid irreversible block when Cd2+ was applied to opened channels, with an apparent blocking rate of ∼3 × 105 M−1s−1. The blocking rate was decreased for channels held at more depolarized voltages that close the channels, which is consistent with the Cd2+ access to this residue being gated from the intracellular side of the channel. 464C channels could be recovered from Cd2+ inhibition in the presence of a dithiol applied to the intracellular side. The rate of this recovery also was reduced when channels were held at depolarized voltages. Finally, Cd2+ could be trapped inside channels that were composed of WT/464C tandem-linked subunits, which could otherwise recover spontaneously from Cd2+ inhibition. Thus, Cd2+ escape is also gated at the intracellular side of the channel. Together, these results are consistent with a voltage-controlled structure at the intracellular side of the spHCN channel that can gate the flow of cations through the pore.