Term Depression Research Articles

Neurotrophin-3 Rescues Striatal Synaptic Plasticity in Model of Neurodegeneration by PLC Signaling Activation.

Neurotrophins are essential factors for neural growth and function; they play a crucial role in neurodegenerative diseases where their expression levels are altered. Our previous research has demonstrated changes in synaptic plasticity and neurotrophin expression levels in a pharmacological model of Huntington's disease (HD) induced by 3-nitropropionic acid (3-NP). In the 3-NP-induced HD model, corticostriatal Long Term Depression (LTD) was impaired, but neurotrophin- 3 (NT-3) restored striatal LTD. This study delves into the NT-3-induced signaling pathways involved in modulating and restoring striatal synaptic plasticity in cerebral slices from 3-NPinduced striatal degeneration in mice in vivo. Phospholipase C (PLC), phosphatidylinositol-3-kinase (PI3K), and mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) pathways activated by NT-3 were analyzed by means of field electrophysiological recordings in brain slices from control and 3-NP treated in the presence of specific inhibitors of the signaling pathways. Using specific inhibitors, PLC, PI3K, and MEK/ERK signaling pathways contribute to NT-3-mediated plasticity modulation in striatal tissue slices recorded from control animals. However, in the neurodegeneration model induced by 3-NP, the recovery of striatal LTD induced by NT-3 was prevented only by the PLC inhibitor. Moreover, the PLC signaling pathway appeared to trigger downstream activation of the endocannabinoid system, evidenced by AM 251, an inhibitor of the CB1 receptor, also hindered NT-3 plasticity recovery. Our finding highlights the specific involvement of the PLC pathway in the neuroprotective effects of NT-3 in mitigating synaptic dysfunction under neurodegenerative conditions.

Inter‐Ion Mutual Repulsion Control for Nonvolatile Artificial Synapse

AbstractOrganic electrochemical transistors (OECTs) are promising candidates for artificial synapses to achieve high‐performance synaptic characteristics. While most research has focused on modifying the properties of organic semiconductors for efficient ion doping, there is a lack of systematic investigation into the relationship between ion‐mediated mechanisms and synaptic performance. In this study, an effective strategy for enhancing electrochemical doping and de‐doping by utilizing different coulombic anions is proposed. The findings reveal that doped ions in the channel layer affect inter‐ion interactions, influencing the non‐volatile effects by improving the doping performance of the synaptic device. Moreover, electrochemical analysis indicates that ions in the channel layer are sequentially de‐doped, enabling high linearity and symmetry. The fabricated devices demonstrate high‐performance synaptic properties including a retention time of ≈102 s with ≈50% retention over peak current and near‐ideal long‐term potentiation/long‐term depression (LTP/LTD) through effective electrochemical doping and de‐doping. These results show that controlling both the properties of organic semiconductors and ion interactions in the electrolyte is crucial for OECTs, opening up various applications for neuromorphic computing.

Flexible Artificial Ag NPs:a-SiC0.11:H Synapse on Al Foil with High Uniformity and On/Off Ratio for Neuromorphic Computing.

A neuromorphic computing network based on SiCx memristor paves the way for a next-generation brain-like chip in the AI era. Up to date, the SiCx-based memristor devices are faced with the challenge of obtaining flexibility and uniformity, which can push forward the application of memristors in flexible electronics. For the first time, we report that a flexible artificial synaptic device based on a Ag NPs:a-SiC0.11:H memristor can be constructed by utilizing aluminum foil as the substrate. The device exhibits stable bipolar resistive switching characteristic even after bending 1000 times, displaying excellent flexibility and uniformity. Furthermore, an on/off ratio of approximately 107 can be obtained. It is found that the incorporation of silver nanoparticles significantly enhances the device's set and reset voltage uniformity by 76.2% and 69.7%, respectively, which is attributed to the contribution of the Ag nanoparticles. The local electric field of Ag nanoparticles can direct the formation and rupture of conductive filaments. The fitting results of I-V curves show that the carrier transport mechanism agrees with Poole-Frenkel (P-F) model in the high-resistance state, while the carrier transport follows Ohm's law in the low-resistance state. Based on the multilevel storage characteristics of the Al/Ag NPs:a-SiC0.11:H/Al foil resistive switching device, we successfully observed the biological synaptic characteristics, including the long-term potentiation (LTP), long-term depression (LTD), and spike-timing-dependent plasticity (STDP). The flexible artificial Ag NPs:a-SiC0.11:H/Al foil synapse possesses excellent conductance modulation capabilities and visual learning function, demonstrating the promise of application in flexible electronics technology for high-efficiency neuromorphic computing in the AI period.

Stress and Depression: Are they Really Related?

the term depression is commonly used to justify the emotional isolation. Common people do not see it as any different from stress or anxiety. Even emotional ventilation, such as crying, is sometimes said to be depression. I often hear suggestions of ventilating one’s feelings or performing leisure activities to get rid of depression. Although, the importance of emotional ventilation can never be understated in order to manage mental health, according to the WHO, depression is a mental disorder that is identified by a loss of pleasure or interest in daily activities for a long period of time, the causes of which may vary from physical or emotional abuse to severe losses in life. Depression needs to be diagnosed and treated, whereas the misuse of the term may lead to misidentification and the illusion that talking to loved ones and getting indulged in one’s favourite activities can cure it.

Distinct synaptic mechanisms drive the behavioral response to acute stress and rapid correction by ketamine

Prevailing hypotheses on the mechanisms of antidepressant action posit that antidepressants directly counteract deficiencies in major neurotransmitter signaling systems that underlie depression. The rapidly acting antidepressant ketamine has been postulated to correct excess glutamatergic signaling via glutamatergic antagonism leading to the rescue of neuronal structural deficits and reversal of behavioral symptoms. We studied this premise using systemic administration of the acetylcholinesterase inhibitor physostigmine, which has been shown to rapidly elicit a shorter-term period of depressed mood in humans via cholinergic mechanisms. We observed that physostigmine induces acute stress in tandem with long term depression of glutamate release in the hippocampus of mice. However, ketamine rapidly acts to re-establish glutamatergic synaptic efficacy via postsynaptic signaling and behaviorally masks the reduction in passive coping induced by physostigmine. These results underscore the divergence of synaptic signaling mechanisms underlying mood changes and antidepressant action and highlight how distinct synaptic mechanisms may underlie neuropsychiatric disorders versus their treatment.

Profiling the neuroimmune cascade in 3xTg-AD mice exposed to successive mild traumatic brain injuries

Repetitive mild traumatic brain injuries (rmTBI) sustained within a window of vulnerability can result in long term cognitive deficits, depression, and eventual neurodegeneration associated with tau pathology, amyloid beta (Aβ) plaques, gliosis, and neuronal and functional loss. However, a comprehensive study relating acute changes in immune signaling and glial reactivity to neuronal changes and pathological markers after single and repetitive mTBIs is currently lacking. In the current study, we addressed the question of how repeated injuries affect the brain neuroimmune response in the acute phase of injury (< 24 h) by exposing the 3xTg-AD mouse model of tau and Aβ pathology to successive (1x-5x) once-daily weight drop closed-head injuries and quantifying immune markers, pathological markers, and transcriptional profiles at 30 min, 4 h, and 24 h after each injury. We used young adult 2–4 month old 3xTg-AD mice to model the effects of rmTBI in the absence of significant tau and Aβ pathology. We identified pronounced sexual dimorphism in this model, with females eliciting more diverse changes after injury compared to males. Specifically, females showed: (1) a single injury caused a decrease in neuron-enriched genes inversely correlated with inflammatory protein expression and an increase in AD-related genes within 24 h, (2) each injury significantly increased a group of cortical cytokines (IL-1α, IL-1β, IL-2, IL-9, IL-13, IL-17, KC) and MAPK phospho-proteins (phospho-Atf2, phospho-Mek1), several of which co-labeled with neurons and correlated with phospho-tau, and (3) repetitive injury caused increased expression of genes associated with astrocyte reactivity and macrophage-associated immune function. Collectively our data suggest that neurons respond to a single injury within 24 h, while other cell types, including astrocytes, transition to inflammatory phenotypes within days of repetitive injury.

Memory device based on MoS2-polyvinyl alcohol for simulating synaptic behavior

A memory device based on MoS2-polyvinyl alcohol was fabricated. As a good dispersant, polyvinyl alcohol solution can disperse 2D layered materials more evenly in the solution. The 19 states of the device conductance are modulated step by step by direct current scanning, which makes it possible to perform the computing task in memory. Then, the presence of conductive filaments allows the resistance state of the memristor to be dynamically transformed, which is similar to some basic behavior of biological synapses. Further, a variety of conductivity states such as short-term potentiation, short term depression, long term potentiation and long-term depression behavior are modulated by applying voltage to simulate the basic behavior of biological synapses. Finally, the paired pulse facilitation, paired pulse depression, spiking timing dependent plasticity and spiking voltage dependent plasticity behaviors of biological synapses are simulated in memristor devices.

Spike rate dependent synaptic characteristics in lamellar, multilayered alpha-MoO3 based two-terminal devices - efficient way to control the synaptic amplification.

Brain-inspired computing systems require a rich variety of neuromorphic devices using multi-functional materials operating at room temperature. Artificial synapses which can be operated using optical and electrical stimuli are in high demand. In this regard, layered materials have attracted a lot of attention due to their tunable energy gap and exotic properties. In the current study, we report the growth of layered MoO3 using the chemical vapor deposition (CVD) technique. MoO3 has an energy gap of 3.22 eV and grows with a large aspect ratio, as seen through optical and scanning electron microscopy. We used transmission electron microscopy (TEM) and X-ray photoelectron spectroscopy for complete characterisation. The two-terminal devices using platinum (Pt/MoO3/Pt) exhibit superior memory with the high-resistance state (HRS) and low-resistance state (LRS) differing by a large resistance (∼MΩ). The devices also show excellent synaptic characteristics. Both optical and electrical pulses can be utilised to stimulate the synapse. Consistent learning (potentiation) and forgetting (depression) curves are measured. Transition from long term depression to long term potentiation can be achieved using the spike frequency dependent pulsing scheme. We have found that the amplification of postsynaptic current can be tuned using such frequency dependent spikes. This will help us to design neuromorphic devices with the required synaptic amplification.

Glial and neuronal mechanisms contributing to differential risks in TREM2 R47H and R62H variants in Alzheimer’s Disease

AbstractBackgroundCoding variants in the microglial TREM2 ectodomain differentially (R47H&gt; R62H) increase the risk of Alzheimer’s disease (AD). To define mechanisms responsible in glia and neurons, we aimed to characterise neuropathology and transcriptomic responses in heterozygotes for these TREM2 variant alleles and for common allele homozygotes (CV) in non‐diseased (n = 16) and AD (n = 42) brain cortical tissue from 58 donors.MethodUsing immunohistochemistry (IHC) and imaging mass cytometry (IMC), we characterised neocortical b‐amyloid and AT8/PHF1 pTau pathology with CV (n = 30) and the R47H (n = 11) or R62H (n = 17) TREM2 carriers. We performed single nuclear RNA sequencing to test for the differential gene expression (DGE) in TREM2 and CV cortical tissues with greater 4G8+ b‐amyloid‐ or PHF1+ pTau‐immunostaining.ResultThere was a two‐fold increase in 4G8+, a three‐fold reduction in AT8+ but no change in PHF1+ immunostaining with AD in both variants versus CV. We found a reduced expression of genes associated with TREM2 function in R47H carriers relative to CV however enhanced microglial activation in R62H carriers. This was associated with an up‐regulation of pathways such as ‘neuroinflammation signalling pathway’ in R62H not seen in R47H. CV astrocytes had little DGE with increasing pathology however both variants (R47H&gt;R62H) had an increased proportion of differentially expressed genes suggestive of a heightened activation state. R47H and R62H astrocytes impacted pathways had opposing actions such as ‘synaptogenesis signalling pathway’ and ‘PDGF signalling’ pathways downregulated in R47H but upregulated in R62H. Neuronal gene expression changes were evident in all variants, however greatly enhanced in R47H in response to 4G8+ b‐amyloid. With increasing PHF1+ pTau gene expression changes were mainly seen in R47H. Excitatory and inhibitory neurons both exhibited DGE in R47H carriers and impacted pathways centred around those involved in ‘synaptogenesis signalling pathway’, ‘SNARE signalling pathway’ and ‘synaptic long term depression’.ConclusionThis analysis identified novel disease‐associated transcriptomic differences in the glial response to TREM2 and the secondary neuronal responses that can explain differences in the genetic AD risk conferred by these two TREM2 risk variants.

Early loss of astrocyte p38alpha MAPK has sexually dimorphic impacts on measures of neuronal excitability and cytokines in aged mice

AbstractBackgroundThe p38alpha MAPK (p38) signaling pathway is ubiquitously expressed in the brain where it plays central roles in neuroinflammation, metabolism, synaptic development and communication, and modulation of blood brain barrier integrity. Its activity in astrocytes has largely been described as immunomodulatory; however, it has also recently been reported to contribute to long term depression and associated behaviors. Astrocytes are also known to be important to healthy brain aging and neuroprotection, but the specific involvement of astrocytic p38 signaling is unclear. We therefore used conditional KO mice to determine how the loss of p38 in astrocytes early in adulthood (3 months) affects synaptic function and cytokine expression phenotypes in later life (20+ months).MethodMice were bred homozygous for floxed p38, heterozygous for a Rosa reporter, and with or without tamoxifen‐inducible Cre recombinase under control of the astrocyte aldh1l1 promoter. When animals were about 3 months of age they were placed on tamoxifen diet (400 ppm) for 4 weeks, after which they were returned to standard chow and allowed to age until 20‐24 months prior to undergoing electrophysiological endpoints or collection of brain tissue for biochemical analyses. Electrically evoked field excitatory post synaptic potentials (fEPSPs) were recorded in hippocampal CA1 stratum radiatum in acutely prepared brain slices and cytokines from the whole hippocampus were measured from a subset of mice that did not undergo electrophysiological recordings.ResultMales and females showed baseline differences in measures of I/O, fiber volley amplitude, early vs. late potentiation, and paired pulse facilitation. Additionally, knockout of astrocyte p38 generally had opposite effects on these parameters in males and females. Interestingly, the pattern of hippocampal IL‐1β cytokine levels mirrored these differences.ConclusionThese data indicate that there may be qualitative differences in male versus female brain aging that are differentially impacted by astrocyte p38 signaling. The implications of these findings are currently being explored to determine the underlying mechanisms for these sexually dimorphic effects and further determine what functional differences may exist for hippocampal‐dependent behaviors.

Electrophysiological variability as marker of dystonia worsening under deep brain stimulation successive withdrawal and renewal effects

DBS has been shown to be an effective intervention for neurological disorders. However, the intervention is complex and many aspects have not been understood. Various clinical situations have no solution and follow trial and error approaches. Dystonia is a movement disorder characterized by involuntary muscle contractions, which gives rise to abnormal movements and postures. Status dystonicus (SD) represents a life-threatening condition that requires urgent assessment and management. Electrophysiological markers for risk of symptom worsening and SD related patterns of evolution in patients treated with long-term deep brain stimulation (DBS), and specially under the effect of withdrawal and renewals of simulation are needed. To this end, we study the variability of neural synchronization as a mechanism for symptom generation under successive perturbations to a system, i.e. withdrawals and renewals of neuromodulation, through computational simulation of clinical profiles under different plasticity conditions. The simulation shows that the neuroplasticity makeup influences the variability of oscillation synchronization patterns in virtual “patients”. The difference between the effect of different electrophysiological signatures is remarkable and under a certain condition (equal medium long term potentiation and long term depression) the situation resembles that of a stable equilibrium, putatively making the sudden worsening or change less likely. Stability of variability can only be observed in this condition and is clearly distinct from other scenarios. ConclusionOur results demonstrate that the neuroplasticity makeup affects the variability of the oscillatory synchrony. This i) informs the shaping of the electrophysiological makeup and ii) might serve as a marker for clinical behavior.

Reverse engineering information processing in lateral amygdala during auditory tones.

Learning in the mammalian lateral amygdala (LA) during auditory fear conditioning (tone - foot shock pairing), one form of associative learning, requires N-methyl-D-aspartate (NMDA) receptor-dependent plasticity. Despite this fact being known for more than two decades, the biophysical details related to signal flow and the involvement of the coincidence detector, NMDAR, in this learning, remain unclear. Here we use a 4000-neuron computational model of the LA (containing two types of pyramidal cells, types A and C, and two types of interneurons, fast spiking FSI and low-threshold spiking LTS) to reverse engineer changes in information flow in the amygdala that underpin such learning; with a specific focus on the role of the coincidence detector NMDAR. The model also included a Ca2s based learning rule for synaptic plasticity. The physiologically constrained model provides insights into the underlying mechanisms that implement habituation to the tone, including the role of NMDARs in generating network activity which engenders synaptic plasticity in specific afferent synapses. Specifically, model runs revealed that NMDARs in tone-FSI synapses were more important during the spontaneous state, although LTS cells also played a role. Training trails with tone only also suggested long term depression in tone-PN as well as tone-FSI synapses, providing possible hypothesis related to underlying mechanisms that might implement the phenomenon of habituation.

The Term depression in Contemporary Lithuanian Journalism

The article attempts to look into the ways that the special meaning of the term depression (Lith. depresija) changes in the discourse of journalism and the factors that drive those changes. Analysis of nearly 2,000 sentences featured in the Corpus of the Contemporary Lithuanian Language that contain the term depression has shown that only one meaning of this term (medical) undergoes transformation as the term transcends the boundaries of a special field, while the rest of its meanings are not susceptible to change. First, the terminological meanings in which this term is used in the material covered by the analysis basically do not change at all, and no break between the term and the underlying concept occurs. Second, the terminological (medical) meaning changes to an extent, and the concept becomes simplified. Third, the terminological meaning undergoes a series of different semantic transformations and the term becomes even more detached from the special meaning, acquiring a number of emotional, expressive shades. These transformations depend on the topics covered by texts, the intentions of the authors, the contextual partners (adjectives, verbs), which often carry some stylistic connotations. Still, it can be sometimes difficult to determine the extent of transformation of the terminological meaning of the term depression with a high degree of accuracy. At times, the boundary between the term depression and the word depression becomes unclear.

A A Spiking Model of Cell Assemblies: Short Term and Associative Memory

Cell Assemblies are the neural basis of both long and short term memories. Cell Assemblies, whose neurons persistently fire, are active short term memories while the neurons are firing, and the memory ceases to be active when the neurons stop firing. This paper provides simulations of excitatory spiking neurons with small world topologies that persist for several hundred milliseconds. Extending this model to include short term depression allows the Cell Assemblies to persist for several seconds, a reasonable psychological duration. These Cell Assemblies are combined in a simple associative memory so that when three Cell Assemblies are associated, ignition of two causes the third to ignite, while pairs of un-associated Cell Assemblies do not lead to the ignition of other Cell Assemblies. This mechanism has a larger capacity than a Hopfield net. The simulations provide a simple neurally based simulation model of short term and associative memory. A discussion of the current psychological theories, other mechanisms for short term memory, the strengths and weaknesses of the paper's simulated models, and proposed challenges are also provided.

Interneuronal network model of theta-nested fast oscillations predicts differential effects of heterogeneity, gap junctions and short term depression for hyperpolarizing versus shunting inhibition.

Theta and gamma oscillations in the hippocampus have been hypothesized to play a role in the encoding and retrieval of memories. Recently, it was shown that an intrinsic fast gamma mechanism in medial entorhinal cortex can be recruited by optogenetic stimulation at theta frequencies, which can persist with fast excitatory synaptic transmission blocked, suggesting a contribution of interneuronal network gamma (ING). We calibrated the passive and active properties of a 100-neuron model network to capture the range of passive properties and frequency/current relationships of experimentally recorded PV+ neurons in the medial entorhinal cortex (mEC). The strength and probabilities of chemical and electrical synapses were also calibrated using paired recordings, as were the kinetics and short-term depression (STD) of the chemical synapses. Gap junctions that contribute a noticeable fraction of the input resistance were required for synchrony with hyperpolarizing inhibition; these networks exhibited theta-nested high frequency oscillations similar to the putative ING observed experimentally in the optogenetically-driven PV-ChR2 mice. With STD included in the model, the network desynchronized at frequencies above ~200 Hz, so for sufficiently strong drive, fast oscillations were only observed before the peak of the theta. Because hyperpolarizing synapses provide a synchronizing drive that contributes to robustness in the presence of heterogeneity, synchronization decreases as the hyperpolarizing inhibition becomes weaker. In contrast, networks with shunting inhibition required non-physiological levels of gap junctions to synchronize using conduction delays within the measured range.

THE EXISTING LANDSCAPE OF DEPRESSION: REVIEW

Introduction: Depression is a global health problem that has been increasing in recent years, but it is still underdiagnosed and it’s not taken seriously enough. For this reason, it is vital for health workers to know their correct diagnosis and treatment to prevent patients from reaching their worst outcome, which is suicide. Objective: To examine how these patients have been approached and managed, and the effectiveness of both pharmacological and non-pharmacological therapies, based on review articles from the last five years. Methodology: a total of 43 original and review articles, collected from the Cochrane Library, PubMed and Google Scholar databases, were searched for the term Depression. The documents were found in Spanish and English. Some articles were excluded due to lack of updated information and lack of relevance for our literature review. Results: there is a fundamental pillar for the treatment of depression, based on psychological therapies (primary and fundamental element), pharmacotherapy and, as a last line, electroconvulsive therapy. The drugs generally used are serotonin reuptake inhibitors and serotonin and noradrenaline reuptake inhibitors. There are other therapies such as acupuncture, music therapy, which have shown some benefit. Conclusions: throughout this time, it has been determined that current diagnostic modalities have made it possible to diagnose early and a greater number of people suffering from depression, starting with psychotherapy, and administering antidepressant drugs in the absence of response to psychotherapy. KEY WORDS: depression, dysthymia, psychotherapy, Serotonin Uptake Inhibitors, Serotonin and Norepinephrine Reuptake Inhibitors.

Sex-related differences in somatic plasticity and possible role of ERK1/2: An in-vivo study of young-adult rats

The present study investigates sex differences in hippocampal functions in the context of synaptic plasticity, which is the cellular basis of learning and memory, and differences in the mitogen-activated protein kinase (MAPK) pathway that accompanies plasticity in young-adult rats. The long-term potentiation (LTP) and long-term depression (LTD) were induced by stimulating the perforant pathway (PP) and field potentials composed of the field excitatory post-synaptic potential (fEPSP) and population spike (PS) were recorded from the dentate gyrus (DG). Following the completion of the electrophysiological recordings, the hippocampi were removed bilaterally, and the protein and gene expression levels of the extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK) and P38-MAPK were determined by Western blot analysis and real-time PCR, respectively. No significant difference was found in synaptic and neuronal function before (basal) and after high-frequency stimulation between male and female rats. Nevertheless, female, but not male, rats were able to express long term depression at the PP – DG synapses, suggesting that sex differences in plasticity are stimulation paradigm specific. MAPK1 expression was higher in males and MAPK3 expression was higher in females, but these differences disappeared after induction of plasticity in both sexes. While the expression of MAPK8 is influenced by sex, independent of the induction of plasticity, MAPK14 expression was down regulated by plasticity induction in females, but not males. No effect of sex, HFS and LFS on total and phosphorylated levels of MAPKs was found except phosphorylated ERK1/2. Phosphorylation of ERK1/2 was up regulated after LFS in male rats but did not change in female rats. These findings indicate that LFS-induced plasticity is differentially modulated between sexes, probably as a result of increased activation of ERK1/2 in male rats.

A realist process evaluation of the INtegrating DEPrEssioN and Diabetes treatmENT (INDEPENDENT) randomized controlled trial in India

AimsWe aimed to determine what key resources, mechanisms, and contextual factors are necessary to integrate depression and diabetes treatment into low-resource settings. MethodsA realist evaluation framework was employed to conduct a comparative case study. Data were collected through document review, key informant interviews (n=4), activity logs, and interviews with implementing health care providers (n=11) to test and refine program theories for collaborative care. ResultsEfforts to enhance patient care coordination (i.e., adapting clinics’ patient flow and resources, on-going trainings, and on-site support for care coordinators) improved implementation of depression treatment by usual care diabetes physicians. Clinician's avoidance of the term depression was identified as a barrier to mental health counseling and treatment. ConclusionsThe variations in organizational features and processes linked to implementation activities across two clinics provided an opportunity to examine how and why different contextual factors help or hinder the implementation process. Findings from this study demonstrate that successful implementation of an integrated depression and diabetes care model is feasible in a low-resource setting, while the revised program theories provide an explanatory framework of coordinated care implementation processes that can inform future efforts to disseminate and scale this care model.

A Floating‐Gate‐Like Transistor Based on InSe vdW Heterostructure with High‐Performance Synaptic Characteristics

With the arrival of the “von Neumann bottleneck,” neuromorphic systems are receiving a lot of attention from scholars as an innovative technology by mimicking the massive parallelism and low‐power operation of the human brain. Herein, a floating‐gate‐like device constructed by the InSe/hBN/O2‐hBN van der Waals heterostructure, where the defective O2‐hBN plays the central role to trap charges, is proposed. This well‐designed device is proved to realize the synaptic functions under UV laser irradiation, such as short‐term plasticity (STP), long‐term plasticity (LTP), paired‐pulse facilitation (PPF), and long‐term potentiation/long‐term depression (LTP/LTD). Especially, the synaptic weight of excitatory postsynaptic current (EPSC) reaches as high as 104%, it reaches the highest standard of this kind of device in recent years, and remains above 300% synaptic weight after 200 s, thus successfully imitating the LTP in biological synapses. The key factors of LTP/LTD curves are overall excellent and can be optimized with input pulses: nonlinearity value can reach 3.32/2.35, and Gmax/Gmin above 10 is achieved. The InSe floating‐gate‐like device with O2‐hBN layer provides an alternative for better and more practical synaptic performances in the field of neuromorphic architectures based on 2D materials.

Back-End, CMOS-Compatible Ferroelectric FinFET for Synaptic Weights

Building Artificial Neural Network accelerators by implementing the vector-matrix multiplication in the analog domain relies on the development of non-volatile and tunable resistances. In this work, we describe the nanofabrication of a three-dimensional HZO—WOx Fin Ferroelectric Field Effect Transistor (FinFeFET) with back-end-of-line conditions. The metal-oxide channel (WOx) is structured into fins and engineered such that: 1) the current-voltage characteristic is linear (Ohmic conduction) and 2) the carrier density is small enough such that the screening length is comparable to one dimension of the device. The process temperature, including the HZO crystallization, does not exceed 400°C. Resistive switching is demonstrated in FinFeFET devices with fins dimension as small as 10 nm wide and 200 nm long. Devices containing a single fin that are 10 nm wide are characterized: 5 µs long voltage pulses in the range (−5.5 and 5 V) are applied on the gate, resulting in analog and symmetric long term potentiation and depression with linearity coefficients of 1.2 and −2.5.