Highly durable and flexible gallium-based oxide conductive-bridging random access memory.

The flexible conductive-bridging random access memory (CBRAM) device using a Cu/TiW/Ga2O3/Pt stack is fabricated on polyimide substrate with low thermal budget process. The CBRAM devices exhibit good memory-resistance characteristics, such as good memory window (>105), low operation voltage, high endurance (>1.4 × 102 cycles), and large retention memory window (>105). The temperature coefficient of resistance in the filament confirms that the conduction mechanism observed in the Ga2O3 layer is similar with the phenomenon of electrochemical metallization (ECM). Moreover, the performance of CBRAM device will not be impacted during the flexibility test. Considering the excellent performance of the CBRAM device fabricated by low-temperature process, it may provide a promising potential for the applications of flexible integrated electronic circuits.

Performance Enhancement for Tungsten-Doped Indium Oxide Thin Film Transistor by Hydrogen Peroxide as Cosolvent in Room-Temperature Supercritical Fluid Systems.

In this study, hydrogen peroxide (H2O2) cosolvent, which was dissolved into supercritical-phase carbon dioxide fluid (SCCO2), is employed to passivate excessive oxygen vacancies of the high-mobility tungsten-doped indium oxide without any essential thermal process. With the detailed material analysis, the internal physical mechanism of the cosolvent effect or the interaction between the cosolvent solution and supercritical-phase fluid is well discussed. In addition, the optimized result has been applied for the thin film transistor device fabrication. As a result, the device with SCCO2 + H2O2 treatment exhibits the lowest subthreshold swing of 82 mV/dec, the lowest interface trap density of 8.76 × 1011 eV-1 cm-2, the lowest hysteresis of 47 mV, and an excellent reliability and uniformity characteristic compared with any other control groups. Besides, an extremely high field-effect mobility of 98.91 cm2/V s can also be observed, while there is even a desirable positive shift for the threshold voltage. Notably, compared with the untreated sample, the highest on/off current ratio of 5.11 × 107 can be achieved with at least four orders of magnitude enhancement by this unique treatment.

Mobility enhancement for high stability tungsten-doped indium-zinc oxide thin film transistors with a channel passivation layer.

This study investigates the electrical characteristics and physical analysis for an amorphous tungsten-doped indium-zinc oxide thin film transistor with different backchannel passivation layers (BPLs), which were deposited by an ion bombardment-free process. A 10 times increase in mobility was observed and attributed to the generation of donor-like oxygen vacancies at the backchannel, which is induced by the oxygen desorption and Gibbs free energy of the BPL material. The mechanism was well studied by XPS analysis. On the other hand, a HfO2 gate insulator was applied for the InWZnO TFT device to control the extremely conductive channel and adjust the negative threshold voltage. With both a HfO2 gate insulator and a suitable BPL, the InWZnO TFT device exhibits good electrical characteristics and a remarkable lifetime when exposed to the ambient air.

ASIC-dependent LTP at multiple glutamatergic synapses in amygdala network is required for fear memory.

Genetic variants in the human ortholog of acid-sensing ion channel-1a subunit (ASIC1a) gene are associated with panic disorder and amygdala dysfunction. Both fear learning and activity-induced long-term potentiation (LTP) of cortico-basolateral amygdala (BLA) synapses are impaired in ASIC1a-null mice, suggesting a critical role of ASICs in fear memory formation. In this study, we found that ASICs were differentially expressed within the amygdala neuronal population, and the extent of LTP at various glutamatergic synapses correlated with the level of ASIC expression in postsynaptic neurons. Importantly, selective deletion of ASIC1a in GABAergic cells, including amygdala output neurons, eliminated LTP in these cells and reduced fear learning to the same extent as that found when ASIC1a was selectively abolished in BLA glutamatergic neurons. Thus, fear learning requires ASIC-dependent LTP at multiple amygdala synapses, including both cortico-BLA input synapses and intra-amygdala synapses on output neurons.

Acid-sensing ion channel-1a is not required for normal hippocampal LTP and spatial memory.

Acid-sensing ion channel-1a (ASIC1a) is localized in brain regions with high synaptic density and is thought to contribute to synaptic plasticity, learning, and memory. A prominent hypothesis is that activation of postsynaptic ASICs promotes depolarization, thereby augmenting N-methyl-d-aspartate receptor function and contributing to the induction of long-term potentiation (LTP). However, evidence for activation of postsynaptic ASICs during neurotransmission has not been established. Here, we re-examined the role of ASIC1a in LTP in the hippocampus using pharmacological and genetic approaches. Our results showed that a tarantula peptide psalmotoxin, which profoundly blocked ASIC currents in the hippocampal neurons, had no effect on LTP. Similarly, normal LTP was robustly generated in ASIC1a-null mice. A further behavioral analysis showed that mice lacking ASIC1a had normal performance in hippocampus-dependent spatial memory. In summary, our results indicate that ASIC1a is not required for hippocampal LTP and spatial memory. We therefore propose that the role of ASIC1a in LTP and spatial learning should be reassessed.

GABA is depolarizing in hippocampal dentate granule cells of the adolescent and adult rats.

GABAergic signaling in hippocampal pyramidal neurons undergoes a switch from depolarizing to hyperpolarizing during early neuronal development. Whether such a transformation of GABAergic action occurs in dentate granule cells (DGCs), located at the first stage of the hippocampal trisynaptic circuit, is unclear. Here, we use noninvasive extracellular recording to monitor the effect of synaptically released GABA on the DGC population. We find that GABAergic responses in adolescent and adult rat DGCs are still depolarizing from rest. Using a morphologically realistic DGC model, we show that GABAergic action, depending on its precise timing and location, can have either an excitatory or inhibitory role in signal processing in the dentate gyrus.