Short-term Synaptic Plasticity Research Articles

Leucine Carboxyl Methyltransferase 1 Overexpression Protects Against Cognitive and Electrophysiological Impairments in Tg2576 APP Transgenic Mice.

Background:The serine/threonine protein phosphatase, PP2A, is thought to play a central role in the molecular pathogenesis of Alzheimer’s disease (AD), and the activity and substrate specificity of PP2A is regulated, in part, through methylation and demethylation of its catalytic subunit. Previously, we found that transgenic overexpression of the PP2A methyltransferase, LCMT-1, or the PP2A methylesterase, PME-1, altered the sensitivity of mice to impairments caused by acute exposure to synthetic oligomeric amyloid-β (Aβ).Objective:Here we sought to test the possibility that these molecules also controlled sensitivity to impairments caused by chronically elevated levels of Aβ produced in vivo.Methods:To do this, we examined the effects of transgenic LCMT-1, or PME-1 overexpression on cognitive and electrophysiological impairments caused by chronic overexpression of mutant human APP in Tg2576 mice.Results:We found that LCMT-1 overexpression prevented impairments in short-term spatial memory and synaptic plasticity in Tg2576 mice, without altering APP expression or soluble Aβ levels. While the magnitude of the effects of PME-1 overexpression in Tg2576 mice was small and potentially confounded by the emergence of non-cognitive impairments, Tg2576 mice that overexpressed PME-1 showed a trend toward earlier onset and/or increased severity of cognitive and electrophysiological impairments.Conclusion:These data suggest that the PP2A methyltransferase, LCMT-1, and the PP2A methylesterase, PME-1, may participate in the molecular pathogenesis of AD by regulating sensitivity to the pathogenic effects of chronically elevated levels of Aβ.

Study of short-term synaptic plasticity in Ion-Gel gated graphene electric-double-layer synaptic transistors

Multi-terminal electric-double-layer transistors have recently attracted extensive interest in terms of mimicking synaptic and neural functions. In this work, an Ion-Gel gated graphene synaptic transistor was proposed to mimic the essential synaptic behaviors by exploiting the bipolar property of graphene and the ionic conductivity of Ion-Gel. The Ion-Gel dielectrics were deposited onto the graphene film by the spin coating process. We consider the top gate and graphene channel as a presynaptic and postsynaptic terminal, respectively. Basic synaptic functions were successfully mimicked, including the excitatory postsynaptic current (EPSC), the effect of spike amplitude and duration on EPSC, and paired-pulse facilitation (PPF). This work may facilitate the application of graphene synaptic transistors in flexible electronics.

An analytical method to measure the contribution of clear synaptic and dense-core peri-synaptic vesicles to neurotransmitter release from synaptic terminals with two classes of secretory vesicles

Two types of secretory vesicles co-exist at some presynaptic terminals. Clear synaptic vesicles (CSV) release their contents at the synaptic active zone, upon single impulses, while dense-core vesicles (DCV) usually release their contents in the periphery of the terminal upon repetitive stimulation. Part of the transmitter released by DCV diffuses to produce paracrine effects, and part of it reaches the postsynaptic terminal, adding its effect to that of synaptic release. This article presents an analytical method to separate the contribution of CSV and DCV to the postsynaptic responses, based on the kinetics of postsynaptic currents (PSCs). Since stimulation with single presynaptic impulses usually triggers release only from CSV, the kinetics of the resulting PSC can be used as a template to model the postsynaptic response to release from CSV during stimulation trains, accounting for the variations in the amplitude of PSCs due to short-term synaptic plasticity. Subtraction of this model simulation to the total recorded PSC renders the response to DCV peri‑synaptic release, which has slower kinetics. The method can be further simplified by measuring only the amplitudes of the PSC peaks for synaptic release and the integral of the current for peri‑synaptic release.•The postsynaptic current in response to presynaptic release from clear synaptic vesicles is modeled using the kinetics of the PSC in response to single impulses.•The model synaptic response is subtracted from the total recorded PSC to obtain the response to peri‑synaptic release from dense-core vesicles.

Exact neural mass model for synaptic-based working memory.

A synaptic theory of Working Memory (WM) has been developed in the last decade as a possible alternative to the persistent spiking paradigm. In this context, we have developed a neural mass model able to reproduce exactly the dynamics of heterogeneous spiking neural networks encompassing realistic cellular mechanisms for short-term synaptic plasticity. This population model reproduces the macroscopic dynamics of the network in terms of the firing rate and the mean membrane potential. The latter quantity allows us to gain insight of the Local Field Potential and electroencephalographic signals measured during WM tasks to characterize the brain activity. More specifically synaptic facilitation and depression integrate each other to efficiently mimic WM operations via either synaptic reactivation or persistent activity. Memory access and loading are related to stimulus-locked transient oscillations followed by a steady-state activity in the β-γ band, thus resembling what is observed in the cortex during vibrotactile stimuli in humans and object recognition in monkeys. Memory juggling and competition emerge already by loading only two items. However more items can be stored in WM by considering neural architectures composed of multiple excitatory populations and a common inhibitory pool. Memory capacity depends strongly on the presentation rate of the items and it maximizes for an optimal frequency range. In particular we provide an analytic expression for the maximal memory capacity. Furthermore, the mean membrane potential turns out to be a suitable proxy to measure the memory load, analogously to event driven potentials in experiments on humans. Finally we show that the γ power increases with the number of loaded items, as reported in many experiments, while θ and β power reveal non monotonic behaviours. In particular, β and γ rhythms are crucially sustained by the inhibitory activity, while the θ rhythm is controlled by excitatory synapses.

Preserving inhibition with a disinhibitory microcircuit in the retina.

Previously, we found that in the mammalian retina, inhibitory inputs onto starburst amacrine cells (SACs) are required for robust direction selectivity of On-Off direction-selective ganglion cells (On-Off DSGCs) against noisy backgrounds (Chen et al., 2016). However, the source of the inhibitory inputs to SACs and how this inhibition confers noise resilience of DSGCs are unknown. Here, we show that when visual noise is present in the background, the motion-evoked inhibition to an On-Off DSGC is preserved by a disinhibitory motif consisting of a serially connected network of neighboring SACs presynaptic to the DSGC. This preservation of inhibition by a disinhibitory motif arises from the interaction between visually evoked network dynamics and short-term synaptic plasticity at the SAC-DSGC synapse. Although the disinhibitory microcircuit is well studied for its disinhibitory function in brain circuits, our results highlight the algorithmic flexibility of this motif beyond disinhibition due to the mutual influence between network and synaptic plasticity mechanisms.

Modeling Social Sensory Processing During Social Computerized Cognitive Training for Psychosis Spectrum: The Resting-State Approach.

Background: Greater impairments in early sensory processing predict response to auditory computerized cognitive training (CCT) in patients with recent-onset psychosis (ROP). Little is known about neuroimaging predictors of response to social CCT, an experimental treatment that was recently shown to induce cognitive improvements in patients with psychosis. Here, we investigated whether ROP patients show interindividual differences in sensory processing change and whether different patterns of SPC are (1) related to the differential response to treatment, as indexed by gains in social cognitive neuropsychological tests and (2) associated with unique resting-state functional connectivity (rsFC).Methods: Twenty-six ROP patients completed 10 h of CCT over the period of 4–6 weeks. Subject-specific improvement in one CCT exercise targeting early sensory processing—a speeded facial Emotion Matching Task (EMT)—was studied as potential proxy for target engagement. Based on the median split of SPC from the EMT, two patient groups were created. Resting-state activity was collected at baseline, and bold time series were extracted from two major default mode network (DMN) hubs: left medial prefrontal cortex (mPFC) and left posterior cingulate cortex (PCC). Seed rsFC analysis was performed using standardized Pearson correlation matrices, generated between the average time course for each seed and each voxel in the brain.Results: Based on SPC, we distinguished improvers—i.e., participants who showed impaired performance at baseline and reached the EMT psychophysical threshold during CCT—from maintainers—i.e., those who showed intact EMT performance at baseline and sustained the EMT psychophysical threshold throughout CCT. Compared to maintainers, improvers showed an increase of rsFC at rest between PCC and left superior and medial frontal regions and the cerebellum. Compared to improvers, maintainers showed increased rsFC at baseline between PCC and superior temporal and insular regions bilaterally.Conclusions: In ROP patients with an increase of connectivity at rest in the default mode network, social CCT is still able to induce sensory processing changes that however do not translate into social cognitive gains. Future studies should investigate if impairments in short-term synaptic plasticity are responsible for this lack of response and can be remediated by pharmacological augmentation during CCT.

Anticipative Tracking with the Short-Term Synaptic Plasticity of Spintronic Devices

Real-time tracking of high-speed objects in cognitive tasks is challenging in the present artificial intelligence techniques because the data processing and computation are time-consuming resulting in impeditive time delays. A brain-inspired continuous attractor neural network (CANN) can be used to track quickly moving targets, where the time delays are intrinsically compensated if the dynamical synapses in the network have the short-term plasticity. Here, we show that synapses with short-term depression can be realized by a magnetic tunnel junction, which perfectly reproduces the dynamics of the synaptic weight in a widely applied mathematical model. Then, these dynamical synapses are incorporated into one-dimensional and two-dimensional CANNs, which are demonstrated to have the ability to predict a moving object via micromagnetic simulations. This portable spintronics-based hardware for neuromorphic computing needs no training and is therefore very promising for the tracking technology for moving targets.

Electrophysiological and Imaging Calcium Biomarkers of Aging in Male and Female 5×FAD Mice.

Background:In animal models and tissue preparations, calcium dyshomeostasis is a biomarker of aging and Alzheimer’s disease that is associated with synaptic dysfunction, neuritic pruning, and dysregulated cellular processes. It is unclear, however, whether the onset of calcium dysregulation precedes, is concurrent with, or is the product of pathological cellular events (e.g., oxidation, amyloid-β production, and neuroinflammation). Further, neuronal calcium dysregulation is not always present in animal models of amyloidogenesis, questioning its reliability as a disease biomarker.Objective:Here, we directly tested for the presence of calcium dysregulation in dorsal hippocampal neurons in male and female 5×FAD mice on a C57BL/6 genetic background using sharp electrodes coupled with Oregon-green Bapta-1 imaging. We focused on three ages that coincide with the course of amyloid deposition: 1.5, 4, and 10 months old.Methods:Outcome variables included measures of the afterhyperpolarization, short-term synaptic plasticity, and calcium kinetics during synaptic activation. Quantitative analyses of spatial learning and memory were also conducted using the Morris water maze. Main effects of sex, age, and genotype were identified on measures of electrophysiology and calcium imaging.Results:Measures of resting Oregon-green Bapta-1 fluorescence showed significant reductions in the 5×FAD group compared to controls. Deficits in spatial memory, along with increases in Aβ load, were detectable at older ages, allowing us to test for temporal associations with the onset of calcium dysregulation.Conclusion:Our results provide evidence that reduced, rather than elevated, neuronal calcium is identified in this 5×FAD model and suggests that this surprising result may be a novel biomarker of AD.

LGI1 downregulation increases neuronal circuit excitability.

Leucine-rich glioma-inactivated 1 (LGI1) is a secreted transsynaptic protein that interacts presynaptically with Kv1.1 potassium channels and a disintegrin and metalloprotease (ADAM) protein 23, and postsynaptically influences α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors through a direct link with the ADAM22 cell adhesion protein. Haploinsufficiency of LGI1 or autoantibodies directed against LGI1 are associated with human epilepsy, generating the hypothesis that a subacute reduction of LGI1 is sufficient to increase network excitability. We tested this hypothesis in ex vivo hippocampal slices and in neuronal cultures, by subacutely reducing LGI1 expression with shRNA. Injection of shRNA-LGI1 in the hippocampus increased dentate granule cell excitability and low-frequency facilitation of mossy fibers to CA3 pyramidal cell neurotransmission. Application of the Kv1 family blocker, α-dendrotoxin, occluded this effect, implicating the involvement of Kv1.1. This subacute reduction of LGI1 was also sufficient to increase neuronal network activity in neuronal primary culture. These results indicate that a subacute reduction in LGI1 potentiates neuronal excitability and short-term synaptic plasticity, and increases neuronal network excitability, opening new avenues for the treatment of limbic encephalitis and temporal lobe epilepsies.

Differential Short-Term Plasticity of PV and SST Neurons Accounts for Adaptation and Facilitation of Cortical Neurons to Auditory Tones.

Cortical responses to sensory stimuli are strongly modulated by temporal context. One of the best studied examples of such modulation is sensory adaptation. We first show that in response to repeated tones pyramidal (Pyr) neurons in male mouse auditory cortex (A1) exhibit facilitating and stable responses, in addition to adapting responses. To examine the potential mechanisms underlying these distinct temporal profiles, we developed a reduced spiking model of sensory cortical circuits that incorporated the signature short-term synaptic plasticity (STP) profiles of the inhibitory parvalbumin (PV) and somatostatin (SST) interneurons. The model accounted for all three temporal response profiles as the result of dynamic changes in excitatory/inhibitory balance produced by STP, primarily through shifts in the relative latency of Pyr and inhibitory neurons. Transition between the three response profiles was possible by changing the strength of the inhibitory PV→Pyr and SST→Pyr synapses. The model predicted that a unit's latency would be related to its temporal profile. Consistent with this prediction, the latency of stable units was significantly shorter than that of adapting and facilitating units. Furthermore, because of the history-dependence of STP the model generated a paradoxical prediction: that inactivation of inhibitory neurons during one tone would decrease the response of A1 neurons to a subsequent tone. Indeed, we observed that optogenetic inactivation of PV neurons during one tone counterintuitively decreased the spiking of Pyr neurons to a subsequent tone 400 ms later. These results provide evidence that STP is critical to temporal context-dependent responses in the sensory cortex.SIGNIFICANCE STATEMENT Our perception of speech and music depends strongly on temporal context, i.e., the significance of a stimulus depends on the preceding stimuli. Complementary neural mechanisms are needed to sometimes ignore repetitive stimuli (e.g., the tic of a clock) or detect meaningful repetition (e.g., consecutive tones in Morse code). We modeled a neural circuit that accounts for diverse experimentally-observed response profiles in auditory cortex (A1) neurons, based on known forms of short-term synaptic plasticity (STP). Whether the simulated circuit reduced, maintained, or enhanced its response to repeated tones depended on the relative dominance of two different types of inhibitory cells. The model made novel predictions that were experimentally validated. Results define an important role for STP in temporal context-dependent perception.

The cross-talk of energy sensing and mitochondrial anchoring sustains synaptic efficacy by maintaining presynaptic metabolism.

Mitochondria supply ATP essential for synaptic transmission. Neurons face exceptional challenges in maintaining energy homeostasis at synapses. Regulation of mitochondrial trafficking and anchoring is critical for neurons to meet increased energy consumption during sustained synaptic activity. However, mechanisms recruiting and retaining presynaptic mitochondria in sensing synaptic ATP levels remain elusive. Here we reveal an energy signaling axis that controls presynaptic mitochondrial maintenance. Activity-induced presynaptic energy deficits could be rescued by recruiting mitochondria through AMPK-PAK energy signaling pathway. Synaptic activity induces AMPK activation within axonal compartments and AMPK-PAK signaling triggers phosphorylation of myosin-VI, which drives mitochondrial recruitment and syntaphilin-mediated anchoring on presynaptic F-actin. This pathway maintains presynaptic energy supply and calcium clearance during intensive synaptic activity. Disrupting this signaling crosstalk triggers local energy deficits and [Ca2+]i buildup, leading to impaired synaptic efficacy during trains of stimulation, and reduced recovery from synaptic depression after prolonged synaptic activity. Our study reveals a mechanistic crosstalk between energy sensing and mitochondria anchoring to maintain presynaptic metabolism, thus fine-tuning short-term synaptic plasticity and prolonged synaptic efficacy.

Enhanced LTP of population spikes in the dentate gyrus of mice haploinsufficient for neurobeachin

Deletion of the autism candidate molecule neurobeachin (Nbea), a large PH-BEACH-domain containing neuronal protein, has been shown to affect synaptic function by interfering with neurotransmitter receptor targeting and dendritic spine formation. Previous analysis of mice lacking one allele of the Nbea gene identified impaired spatial learning and memory in addition to altered autism-related behaviours. However, no functional data from living heterozygous Nbea mice (Nbea+/−) are available to corroborate the behavioural phenotype. Here, we explored the consequences of Nbea haploinsufficiency on excitation/inhibition balance and synaptic plasticity in the intact hippocampal dentate gyrus of Nbea+/− animals in vivo by electrophysiological recordings. Based on field potential recordings, we show that Nbea+/− mice display enhanced LTP of the granule cell population spike, but no differences in basal synaptic transmission, synapse numbers, short-term plasticity, or network inhibition. These data indicate that Nbea haploinsufficiency causes remarkably specific alterations to granule cell excitability in vivo, which may contribute to the behavioural abnormalities in Nbea+/− mice and to related symptoms in patients.

Synaptic vesicles transiently dock to refill release sites.

Synaptic vesicles fuse with the plasma membrane to release neurotransmitter following an action potential, after which new vesicles must ‘dock’ to refill vacated release sites. To capture synaptic vesicle exocytosis at cultured mouse hippocampal synapses, we induced single action potentials by electrical field stimulation then subjected neurons to high-pressure freezing to examine their morphology by electron microscopy. During synchronous release, multiple vesicles can fuse at a single active zone. Fusions during synchronous release are distributed throughout the active zone, whereas fusions during asynchronous release are biased toward the center of the active zone. After stimulation, the total number of docked vesicles across all synapses decreases by ~40%. Within 14 ms, new vesicles are recruited and fully replenish the docked pool, but this docking is transient and they either undock or fuse within 100 ms. These results demonstrate that recruitment of synaptic vesicles to release sites is rapid and reversible.

Albumen based protein gated bioinspired neuromorphic transistors with learning abilities

The development of bioinspired neuromorphic device is an essential step to build brain-inspired neuromorphic cognitive systems. While sustainable and renewable biomaterial is considered as an essential building block for bioinspired portable neuromorphic device. Here, albumen based protein gated oxide neuromorphic transistors capable of learning activities have been proposed. The albumen-based electrolyte film demonstrates a high specific capacitance of ~1.7 μF/cm 2 at 1.0 Hz. The transistor demonstrates good electrical performances with high ON/OFF ratio of ~7.1 × 10 7 and a field-effect mobility of ~4.5 cm 2 /(V·s). Resistor loaded inverters are obtained by connecting a transistor and a resistor in series. Besides, short-term synaptic plasticities are mimicked on the proposed bioinspired neuromorphic transistor. The transitions from short-term memory to long-term memory and the learning-forgetting-relearning process are also successfully imitated. More importantly, target learning processes demonstrate a novel idea to accelerate the learning activities of neuromorphic transistor. The results indicate potential applications for the proposed bioinspired neuromorphic transistor in green neuromorphic cognitive systems. • Albumen gated bioinspired neuromorphic transistors are fabricated. • The device exhibits good electrical performances and learning abilities. • Learning activities are accelerated based on target learning mechanism.

Theoretical distinction between functional states in working memory and their corresponding neural states

ABSTRACT Working memory (WM) is important for guiding behaviour, but not always for the next possible action. Here we define a WM item that is currently relevant for guiding behaviour as the functionally “active” item; whereas items maintained in WM, but not immediately relevant to behaviour, are defined as functionally “latent”. Traditional neurophysiological theories of WM proposed that content is maintained via persistent neural activity (e.g., stable attractors); however, more recent theories have highlighted the potential role for “activity-silent” mechanisms (e.g., short-term synaptic plasticity). Given these somewhat parallel dichotomies, functionally active and latent cognitive states of WM have been associated with storage based on persistent-activity and activity-silent neural mechanisms, respectively. However, in this article we caution against a one-to-one correspondence between functional and activity states. We argue that the principal theoretical requirement for active and latent WM is that the corresponding neural states play qualitatively different functional roles. We consider a number of candidate solutions, and conclude that the neurophysiological mechanisms for functionally active and latent WM items are theoretically independent of the distinction between persistent activity-based and activity-silent forms of WM storage.

Levetiracetam Reduced the Basal Excitability of the Dentate Gyrus without Restoring Impaired Synaptic Plasticity in Rats with Temporal Lobe Epilepsy.

Temporal lobe epilepsy (TLE), the most common type of focal epilepsy, affects learning and memory; these effects are thought to emerge from changes in synaptic plasticity. Levetiracetam (LEV) is a widely used antiepileptic drug that is also associated with the reversal of cognitive dysfunction. The long-lasting effect of LEV treatment and its participation in synaptic plasticity have not been explored in early chronic epilepsy. Therefore, through the measurement of evoked field potentials, this study aimed to comprehensively identify the alterations in the excitability and the short-term (depression/facilitation) and long-term synaptic plasticity (long-term potentiation, LTP) of the dentate gyrus of the hippocampus in a lithium–pilocarpine rat model of TLE, as well as their possible restoration by LEV (1 week; 300 mg/kg/day). TLE increased the population spike (PS) amplitude (input/output curve); interestingly, LEV treatment partially reduced this hyperexcitability. Furthermore, TLE augmented synaptic depression, suppressed paired-pulse facilitation, and reduced PS-LTP; however, LEV did not alleviate such alterations. Conversely, the excitatory postsynaptic potential (EPSP)-LTP of TLE rats was comparable to that of control rats and was decreased by LEV. LEV caused a long-lasting attenuation of basal hyperexcitability but did not restore impaired synaptic plasticity in the early chronic phase of TLE.

Generalized half-center oscillators with short-term synaptic plasticity.

How can we develop simple yet realistic models of the small neural circuits known as central pattern generators (CPGs), which contribute to generate complex multiphase locomotion in living animals? In this paper we introduce a new model (with design criteria) of a generalized half-center oscillator, (pools of) neurons reciprocally coupled by fast/slow inhibitory and excitatory synapses, to produce either alternating bursting or other rhythmic patterns, characterized by different phase lags, depending on the sensory or other external input. We also show how to calibrate its parameters, based on both physiological and functional criteria and on bifurcation analysis. This model accounts for short-term neuromodulation in a biophysically plausible way and is a building block to develop more realistic and functionally accurate CPG models. Examples and counterexamples are used to point out the generality and effectiveness of our design approach.

A New Approach to the Fabrication of Memristive Neuromorphic Devices: Compositionally Graded Films.

Energy-efficient computing paradigms beyond conventional von-Neumann architecture, such as neuromorphic computing, require novel devices that enable information storage at nanoscale in an analogue way and in-memory computing. Memristive devices with long-/short-term synaptic plasticity are expected to provide a more capable neuromorphic system compared to traditional Si-based complementary metal-oxide-semiconductor circuits. Here, compositionally graded oxide films of Al-doped MgxZn1−xO (g-Al:MgZnO) are studied to fabricate a memristive device, in which the composition of the film changes continuously through the film thickness. Compositional grading in the films should give rise to asymmetry of Schottky barrier heights at the film-electrode interfaces. The g-Al:MgZnO films are grown by using aerosol-assisted chemical vapor deposition. The current-voltage (I-V) and capacitance-voltage (C-V) characteristics of the films show self-rectifying memristive behaviors which are dependent on maximum applied voltage and repeated application of electrical pulses. Endurance and retention performance tests of the device show stable bipolar resistance switching (BRS) with a short-term memory effect. The short-term memory effects are ascribed to the thermally activated release of the trapped electrons near/at the g-Al:MgZnO film-electrode interface of the device. The volatile resistive switching can be used as a potential selector device in a crossbar memory array and a short-term synapse in neuromorphic computing.

Modulation of information processing by AMPA receptor auxiliary subunits.

AMPA-type glutamate receptors (AMPARs) are key molecules of neuronal communication in our brain. The discovery of AMPAR auxiliary subunits, such as proteins of the TARP, CKAMP and CNIH families, fundamentally changed our understanding of how AMPAR function is regulated. Auxiliary subunits control almost all aspects of AMPAR function in the brain. They influence AMPAR assembly, composition, structure, trafficking, subcellular localization and gating. This influence has important implications for synapse function. In the present review, we first discuss how auxiliary subunits affect the strength of synapses by modulating number and localization of AMPARs in synapses as well as their glutamate affinity, conductance and peak open probability. Next we explain how the presence of auxiliary subunits alters temporal precision and integrative properties of synapses by influencing gating kinetics of the receptors. Auxiliary subunits of the TARP and CKAMP family modulate synaptic short-term plasticity by increasing anchoring of AMPARs in synapses and by altering their desensitization kinetics. We then describe how auxiliary subunits of the TARP, CKAMP and CNIH families are involved in Hebbian and homeostatic plasticity, which can be explained by their influence on surface trafficking and synaptic targeting. In conclusion, the series of studies covered in this review show that auxiliary subunits play a pivotal role in controlling information processing in the brain by modulating synaptic computation.

Implementation of Synaptic Device Using Various High-k Gate Dielectric Stacks.

We investigate the characteristics of short-term and long-term synaptic plasticity in a Si-based fieldeffect transistor (FET)-type memory device. An Al₂O₃/HfO₂/Si₃N₄/SiO₂ gate dielectric stack is used to realize short-term and long-term plasticity (STP/LTP). Si₃N₄ and HfO₂ layers are designed to charge trap layer for synaptic device. The mechanism of STP and LTP operation is analyzed by considering the device response to the potentiation and depression pulses and retention measurement of the memory functionality. To investigate the STP operation, paired pulse facilitation (PPF) measurement is performed. The retention characteristic is also studied to validate the LTP property of the device. By investigating a device with an Al₂O₃/HfO₂/Si₃N₄ stack as a control device, it is shown that the Al₂O₃/HfO₂/Si₃N₄/SiO₂ stack device is suitable for a synaptic device in neuromorphic systems.