A Comparison Study on Multilayered Barrier Oxide Structure in Charge Trap Flash for Synaptic Operation

A synaptic device that contains weight information between two neurons is one of the essential components in a neuromorphic system, which needs highly linear and symmetric characteristics of weight update. In this study, a charge trap flash (CTF) memory device with a multilayered high-κ barrier oxide structure on the MoS2 channel is proposed. The fabricated device was oxide-engineered on the barrier oxide layers to achieve improved synaptic functions. A comparison study between two fabricated devices with different barrier oxide materials (Al2O3 and SiO2) suggests that a high-κ barrier oxide structure improves the synaptic operations by demonstrating the increased on/off ratio and symmetry of synaptic weight updates due to a better coupling ratio. Lastly, the fabricated device has demonstrated reliable potentiation and depression behaviors and spike-timing-dependent plasticity (STDP) for use in a spiking neural network (SNN) neuromorphic system.

Maintenance of Synaptic Stability Requires Calcium-Independent Phospholipase A2Activity

Phospholipases A2(PLA2s) represent one of the largest groups of lipid-modifying enzymes. Over the years, significant advances have been made in understanding their potential physiological and pathological functions. Depending on their calcium requirement for activation, PLA2s are classified into calcium dependent and independent. This paper mainly focuses on brain calcium-independent PLA2(iPLA2) and on the mechanisms by which they influence neuronal function and regulate synaptic plasticity. Particular attention will be given to the iPLA2γisoform and its role in the regulation of synaptic glutamate receptors. In particular, the paper discusses the possibility that brain iPLA2γdeficiencies could destabilise normal synaptic operation and might contribute to the aetiology of some brain disorders. In this line, the paper presents new data indicating that iPLA2γdeficiencies accentuate AMPA receptor destabilization and tau phosphorylation, which suggests that this iPLA2isoform should be considered as a potential target for the treatment of Tau-related disorders.