Ferroelectrics have been demonstrated as excellent building blocks for highperformance nonvolatile memories, including memristors, which play critical roles in the hardware implementation of artificial synapses and in-memory computing. Here, it is reported that the emerging van der Waals ferroelectric α-In 2 Se 3 can be used to successfully implement heterosynaptic plasticity (a fundamental but rarely emulated synaptic form) and achieve a resistanceswitching ratio of heterosynaptic memristors above 10 3 , which is two orders of magnitude larger than that in other similar devices. The polarization change of ferroelectric α-In 2 Se 3 channel is responsible for the resistance switching at various paired terminals. The third terminal of α-In 2 Se 3 memristors exhibits nonvolatile control over channel current at a picoampere level, endowing the devices with picojoule read-energy consumption to emulate the associative heterosynaptic learning. The simulation proves that both supervised and unsupervised learning manners can be implemented in α-In 2 Se 3 neutral networks with high image recognition accuracy. Moreover, these heterosynaptic devices can naturally realize Boolean logic without an additional circuit component. The results suggest that van der Waals ferroelectrics hold great potential for applications in complex, energy-efficient, brain-inspired computing systems and logic-in-memory computers.

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during the measurement. To obtain the degradation-free gm, pulsed Id-Vg with a transition time of 6 gs must be used. Lifetime of pMOSFETs is limited by negative bias Fig. 3 also shows that gm actually increases with time temperature instability (NBTI). For the first time, we show under a constant Vgst. This is caused by a reduction of lVgstthat the NBTI-induced threshold voltage shift, AVth, Vthl, which enhances the effective mobility, despite the measured in early works by using either the 'on-the-fly' or the degradation of low-field mobility. A more detailed analysis conventional transfer characteristics extrapolation techniques on the variation of effective mobility during stress was given is not the real AVth under practical operation. A new method in our recent work [7]. After using the degradation-free Id and is proposed for estimating the real AVth.gm, Fig. 4 shows that the AVth(OTF) is more than doubled.However, we will demonstrate that AVth(OTF) is not

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Hundreds of genetic variants in KCNQ2 encoding the voltage-gated potassium channel KV7.2 are associated with early onset epilepsy and/or developmental disability, but the functional consequences of most variants are unknown. Absent functional annotation for KCNQ2 variants hinders identification of individuals who may benefit from emerging precision therapies. We employed automated patch clamp recording to assess at an unprecedented scale the functional and pharmacological properties of 79 missense and 2 inframe deletion KCNQ2 variants. Among the variants we studied were 18 known pathogenic variants, 24 mostly rare population variants, and 39 disease-associated variants with unclear functional effects. We analyzed electrophysiological data recorded from 9,480 cells. The functional properties of 18 known pathogenic variants largely matched previously published results and validated automated patch clamp for this purpose. Unlike rare population variants, most disease-associated KCNQ2 variants exhibited prominent loss-of-function with dominant-negative effects, providing strong evidence in support of pathogenicity. All variants responded to retigabine, although there were substantial differences in maximal responses. Our study demonstrated that dominant-negative loss-offunction is a common mechanism associated with missense KCNQ2 variants. Importantly, we observed genotype-dependent differences in the response of KCNQ2 variants to retigabine, a proposed precision therapy for KCNQ2 developmental and epileptic encephalopathy. Brief Summary -Vanoye, et al. determined the functional consequences and pharmacological responses of 81 KCNQ2 variants with implications for precision therapy of a genetic epilepsy.