Association of connexin36 with adherens junctions at mixed synapses and distinguishing electrophysiological features of those at mossy fiber terminals in rat ventral hippocampus.

BACKGROUND: Granule cells in the hippocampus project axons to hippocampal CA3 pyramidal cells where they form large mossy fiber terminals. We have reported that these terminals contain the gap junction protein connexin36 (Cx36) specifically in the stratum lucidum of rat ventral hippocampus, thus creating morphologically mixed synapses that have the potential for dual chemical/electrical transmission. METHODOLOGY: Here, we used various approaches to characterize molecular and electrophysiological relationships between the Cx36-containing gap junctions at mossy fiber terminals and their postsynaptic elements and to examine molecular relationships at mixed synapses in the brainstem. RESULTS: In rat and human ventral hippocampus, many of these terminals, identified by their selective expression of vesicular zinc transporter-3 (ZnT3), displayed multiple, immunofluorescent Cx36-puncta representing gap junctions, which were absent at mossy fiber terminals in the dorsal hippocampus. In rat, these were found in close proximity to the protein constituents of adherens junctions (i.e., N-cadherin and nectin-1) that are structural hallmarks of mossy fiber terminals, linking these terminals to the dendritic shafts of CA3 pyramidal cells, thus indicating the loci of gap junctions at these contacts. Cx36-puncta were also associated with adherens junctions at mixed synapses in the brainstem, supporting emerging views of the structural organization of the adherens junction-neuronal gap junction complex. Electrophysiologically induced long-term potentiation (LTP) of field responses evoked by mossy fiber stimulation was greater in the ventral than dorsal hippocampus. CONCLUSIONS: The electrical component of transmission at mossy fiber terminals may contribute to enhanced LTP responses in the ventral hippocampus.

Patterns of connexin36 and eGFP reporter expression among motoneurons in spinal sexually dimorphic motor nuclei in mouse.

BACKGROUND: Sexually dimorphic spinal motoneurons (MNs) in the dorsomedial nucleus (DMN) and dorsolateral nucleus (DLN) as well as those in the cremaster nucleus are involved in reproductive behaviours, and the cremaster nucleus additionally contributes to testicular thermoregulation. It has been reported that MNs in DMN and DLN are extensively linked by gap junctions forming electrical synapses composed of connexin36 (Cx36) and there is evidence that subpopulation of MNs in the cremaster nucleus are also electrically coupled by these synapses. METHODOLOGY: We used immunofluorescence methods to detect enhanced green fluorescent protein (eGFP) reporter for Cx36 expression in these motor nuclei. RESULTS: We document in male mice that about half the MNs in each of DMN and DLN express eGFP, while the remaining half do not. Further, we found that the eGFP+ vs. eGFP- subsets of MNs in each of these motor nuclei innervate different target muscles; eGFP+ MNs in DMN and DLN project to sexually dimorphic bulbocavernosus and ischiocavernosus muscles, while the eGFP- subsets project to sexually non-dimorphic anal and external urethral sphincter muscles. Similarly, eGFP+ vs. eGFP- cremaster MNs were found to project to anatomically distinct portions of the cremaster muscle. By immunofluorescence, nearly all motoneurons in both DMN and DLN displayed punctate labelling for Cx36, including at eGFP+/eGFP+, eGFP+/eGFP- and eGFP-/eGFP- cell appositions. CONCLUSIONS: Most if not all motoneurons in DMN and DLN are electrically coupled, including sexually dimorphic and non-dimorphic motoneurons with each other, despite absence of eGFP reporter in the non-dimorphic populations in these nuclei that have selective projections to sexually non-dimorphic target muscles.

SARS-CoV-2 Nucleocapsid Protein Induces Tau Pathological Changes That Can Be Counteracted by SUMO2.

Neurologic manifestations are an immediate consequence of SARS-CoV-2 infection, the etiologic agent of COVID-19, which, however, may also trigger long-term neurological effects. Notably, COVID-19 patients with neurological symptoms show elevated levels of biomarkers associated with brain injury, including Tau proteins linked to Alzheimer's pathology. Studies in brain organoids revealed that SARS-CoV-2 alters the phosphorylation and distribution of Tau in infected neurons, but the mechanisms are currently unknown. We hypothesize that these pathological changes are due to the recruitment of Tau into stress granules (SGs) operated by the nucleocapsid protein (NCAP) of SARS-CoV-2. To test this hypothesis, we investigated whether NCAP interacts with Tau and localizes to SGs in hippocampal neurons in vitro and in vivo. Mechanistically, we tested whether SUMOylation, a posttranslational modification of NCAP and Tau, modulates their distribution in SGs and their pathological interaction. We found that NCAP and Tau colocalize and physically interact. We also found that NCAP induces hyperphosphorylation of Tau and causes cognitive impairment in mice infected with NCAP in their hippocampus. Finally, we found that SUMOylation modulates NCAP SG formation in vitro and cognitive performance in infected mice. Our data demonstrate that NCAP induces Tau pathological changes both in vitro and in vivo. Moreover, we demonstrate that SUMO2 ameliorates NCAP-induced Tau pathology, highlighting the importance of the SUMOylation pathway as a target of intervention against neurotoxic insults, such as Tau oligomers and viral infection.

Excitatory synaptic structural abnormalities produced by templated aggregation of α-syn in the basolateral amygdala.

Parkinson's disease (PD) and Dementia with Lewy bodies (DLB) are characterized by neuronal α-synuclein (α-syn) inclusions termed Lewy Pathology, which are abundant in the amygdala. The basolateral amygdala (BLA), in particular, receives projections from the thalamus and cortex. These projections play a role in cognition and emotional processing, behaviors which are impaired in α-synucleinopathies. To understand if and how pathologic α-syn impacts the BLA requires animal models of α-syn aggregation. Injection of α-syn pre-formed fibrils (PFFs) into the striatum induces robust α-syn aggregation in excitatory neurons in the BLA that corresponds with reduced contextual fear conditioning. At early time points after aggregate formation, cortico-amygdala excitatory transmission is abolished. The goal of this project was to determine if α-syn inclusions in the BLA induce synaptic degeneration and/or morphological changes. In this study, we used C57BL/6 J mice injected bilaterally with PFFs in the dorsal striatum to induce α-syn aggregate formation in the BLA. A method was developed using immunofluorescence and three-dimensional reconstruction to analyze excitatory cortico-amygdala and thalamo-amygdala presynaptic terminals closely juxtaposed to postsynaptic densities. The abundance and morphology of synapses were analyzed at 6- or 12-weeks post-injection of PFFs. α-Syn aggregate formation in the BLA did not cause a significant loss of synapses, but cortico-amygdala and thalamo-amygdala presynaptic terminals and postsynaptic densities with aggregates of α-syn show increased volumes, similar to previous findings in human DLB cortex, and in non-human primate models of PD. Transmission electron microscopy showed that asymmetric synapses in mice with PFF-induced α-syn aggregates have reduced synaptic vesicle intervesicular distances, similar to a recent study showing phospho-serine-129 α-syn increases synaptic vesicle clustering. Thus, pathologic α-syn causes major alterations to synaptic architecture in the BLA, potentially contributing to behavioral impairment and amygdala dysfunction observed in synucleinopathies.

Age-related alterations in efferent medial olivocochlear-outer hair cell and primary auditory ribbon synapses in CBA/J mice.

Introduction: Hearing decline stands as the most prevalent single sensory deficit associated with the aging process. Giving compelling evidence suggesting a protective effect associated with the efferent auditory system, the goal of our study was to characterize the age-related changes in the number of efferent medial olivocochlear (MOC) synapses regulating outer hair cell (OHC) activity compared with the number of afferent inner hair cell ribbon synapses in CBA/J mice over their lifespan. Methods: Organs of Corti of 3-month-old CBA/J mice were compared with mice aged between 10 and 20 months, grouped at 2-month intervals. For each animal, one ear was used to characterize the synapses between the efferent MOC fibers and the outer hair cells (OHCs), while the contralateral ear was used to analyze the ribbon synapses between inner hair cells (IHCs) and type I afferent nerve fibers of spiral ganglion neurons (SGNs). Each cochlea was separated in apical, middle, and basal turns, respectively. Results: The first significant age-related decline in afferent IHC-SGN ribbon synapses was observed in the basal cochlear turn at 14 months, the middle turn at 16 months, and the apical turn at 18 months of age. In contrast, efferent MOC-OHC synapses in CBA/J mice exhibited a less pronounced loss due to aging which only became significant in the basal and middle turns of the cochlea by 20 months of age. Discussion: This study illustrates an age-related reduction on efferent MOC innervation of OHCs in CBA/J mice starting at 20 months of age. Our findings indicate that the morphological decline of efferent MOC-OHC synapses due to aging occurs notably later than the decline observed in afferent IHC-SGN ribbon synapses.

Tau-mediated synaptic dysfunction is coupled with HCN channelopathy.

INTRODUCTION: In tauopathies, altered tau processing correlates with impairments in synaptic density and function. Changes in hyperpolarization-activated cyclic nucleotide-gated (HCN) channels contribute to disease-associated abnormalities in multiple neurodegenerative diseases. METHODS: To investigate the link between tau and HCN channels, we performed histological, biochemical, ultrastructural, and functional analyses of hippocampal tissues from Alzheimer's disease (AD), age-matched controls, Tau35 mice, and/or Tau35 primary hippocampal neurons. RESULTS: Expression of specific HCN channels is elevated in post mortem AD hippocampus. Tau35 mice develop progressive abnormalities including increased phosphorylated tau, enhanced HCN channel expression, decreased dendritic branching, reduced synapse density, and vesicle clustering defects. Tau35 primary neurons show increased HCN channel expression enhanced hyperpolarization-induced membrane voltage "sag" and changes in the frequency and kinetics of spontaneous excitatory postsynaptic currents. DISCUSSION: Our findings are consistent with a model in which pathological changes in tauopathies impact HCN channels to drive network-wide structural and functional synaptic deficits. HIGHLIGHTS: Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are functionally linked to the development of tauopathy. Expression of specific HCN channels is elevated in the hippocampus in Alzheimer's disease and the Tau35 mouse model of tauopathy. Increased expression of HCN channels in Tau35 mice is accompanied by hyperpolarization-induced membrane voltage "sag" demonstrating a detrimental effect of tau abnormalities on HCN channel function. Tau35 expression alters synaptic organization, causing a loosened vesicle clustering phenotype in Tau35 mice.

Multi-scale modelling of location- and frequency-dependent synaptic plasticity induced by transcranial magnetic stimulation in the dendrites of pyramidal neurons.

Background: Repetitive transcranial magnetic stimulation (rTMS) induces long-term changes of synapses, but the mechanisms behind these modifications are not fully understood. Although there has been progress in the development of multi-scale modeling tools, no comprehensive module for simulating rTMS-induced synaptic plasticity in biophysically realistic neurons exists.. Objective: We developed a modelling framework that allows the replication and detailed prediction of long-term changes of excitatory synapses in neurons stimulated by rTMS. Methods: We implemented a voltage-dependent plasticity model that has been previously established for simulating frequency-, time-, and compartment-dependent spatio-temporal changes of excitatory synapses in neuronal dendrites. The plasticity model can be incorporated into biophysical neuronal models and coupled to electrical field simulations. Results: We show that the plasticity modelling framework replicates long-term potentiation (LTP)-like plasticity in hippocampal CA1 pyramidal cells evoked by 10-Hz repetitive magnetic stimulation (rMS). This plasticity was strongly distance dependent and concentrated at the proximal synapses of the neuron. We predicted a decrease in the plasticity amplitude for 5 Hz and 1 Hz protocols with decreasing frequency. Finally, we successfully modelled plasticity in distal synapses upon local electrical theta-burst stimulation (TBS) and predicted proximal and distal plasticity for rMS TBS. Notably, the rMS TBS-evoked synaptic plasticity exhibited robust facilitation by dendritic spikes and low sensitivity to inhibitory suppression. Conclusion: The plasticity modelling framework enables precise simulations of LTP-like cellular effects with high spatio-temporal resolution, enhancing the efficiency of parameter screening and the development of plasticity-inducing rTMS protocols.

Synapse and primary cilia dysfunctions in Autism Spectrum Disorders. Avenues to normalize these functions.

AIM: An update on the plasticity of the brain networks involved in autism (autism spectrum disorders [ASD]), and the increasing role of their synapses and primary non-motile cilia. METHODS: Data from PubMed and Google on this subject, published until February 2024, were analyzed. RESULTS: Structural and functional brain characteristics and genetic particularities involving synapses and cilia that modify neuronal circuits are observed in ASD, such as reduced pruning of dendrites, minicolumnar pathology, or persistence of connections usually doomed to disappear. Proteins involved in synapse functions (such as neuroligins and neurexins), in the postsynaptic architectural scaffolding (such as Shank proteins) or in cilia functions (such as IFT-independent kinesins) are often abnormal. There is an increase in glutaminergic transmission and a decrease in GABA inhibition. ASD may occur in genetic ciliopathies. The means of modulating these specificities, when deemed useful, are described. INTERPRETATION: The wide range of clinical manifestations of ASD is strongly associated with abnormalities in the morphology, functions, and plasticity of brain networks, involving their synapses and non-motile cilia. Their modulation offers important research perspectives on treatments when needed, especially since brain plasticity persists much later than previously thought. Improved early detection of ASD and additional studies on synapses and primary cilia are needed.

A Reconfigurable All-Optical-Controlled Synaptic Device for Neuromorphic Computing Applications.

Retina-inspired visual sensors play a crucial role in the realization of neuromorphic visual systems. Nevertheless, significant obstacles persist in the pursuit of achieving bidirectional synaptic behavior and attaining high performance in the context of photostimulation. In this study, we propose a reconfigurable all-optical controlled synaptic device based on the IGZO/SnO/SnS heterostructure, which integrates sensing, storage and processing functions. Relying on the simple heterojunction stack structure and the role of energy band engineering, synaptic excitatory and inhibitory behaviors can be observed under the light stimulation of ultraviolet (266 nm) and visible light (405, 520 and 658 nm) without additional voltage modulation. In particular, junction field-effect transistors based on the IGZO/SnO/SnS heterostructure were fabricated to elucidate the underlying bidirectional photoresponse mechanism. In addition to optical signal processing, an artificial neural network simulator based on the optoelectrical synapse was trained and recognized handwritten numerals with a recognition rate of 91%. Furthermore, we prepared an 8 × 8 optoelectrical synaptic array and successfully demonstrated the process of perception and memory for image recognition in the human brain, as well as simulated the situation of damage to the retina by ultraviolet light. This work provides an effective strategy for the development of high-performance all-optical controlled optoelectronic synapses and a practical approach to the design of multifunctional artificial neural vision systems.

Kif1a and intact microtubules maintain synaptic-vesicle populations at ribbon synapses in zebrafish hair cells.

Sensory hair cells of the inner ear utilize specialized ribbon synapses to transmit sensory stimuli to the central nervous system. This sensory transmission necessitates rapid and sustained neurotransmitter release, which relies on a large pool of synaptic vesicles at the hair-cell presynapse. Work in neurons has shown that kinesin motor proteins traffic synaptic material along microtubules to the presynapse, but how new synaptic material reaches the presynapse in hair cells is not known. We show that the kinesin motor protein Kif1a and an intact microtubule network are necessary to enrich synaptic vesicles at the presynapse in hair cells. We use genetics and pharmacology to disrupt Kif1a function and impair microtubule networks in hair cells of the zebrafish lateral-line system. We find that these manipulations decrease synaptic-vesicle populations at the presynapse in hair cells. Using electron microscopy, along with in vivo calcium imaging and electrophysiology, we show that a diminished supply of synaptic vesicles adversely affects ribbon-synapse function. Kif1a mutants exhibit dramatic reductions in spontaneous vesicle release and evoked postsynaptic calcium responses. Additionally, we find that kif1a mutants exhibit impaired rheotaxis, a behavior reliant on the ability of hair cells in the lateral line to respond to sustained flow stimuli. Overall, our results demonstrate that Kif1a-based microtubule transport is critical to enrich synaptic vesicles at the active zone in hair cells, a process that is vital for proper ribbon-synapse function.

A Dual-Functional Integration of Photodetectors and Artificial Optoelectronic Synapses on a VO2/WO3 Heterojunction Device.

Bionic visual systems require multimodal integration of eye-like photodetectors and brain-like image memory. However, the integration of photodetectors (PDs) and artificial optoelectronic synapses devices (OESDs) by one device remains a giant challenge due to their photoresponse discrepancy. Herein, a dual-functional integration of PDs and OESDs based on VO2/WO3 heterojunctions is presented. The device can be able to realize a dual-mode conversion between PDs and OESDs through tuning the bias voltage. Under zero bias voltage, the device exhibiting excellent photodetecting behaviors based on the photovoltaic effect, showing a high self-powered photoresponsivity of 18.5 mA W-1 and high detectivity of 7.5 × 1010 Jones with fast photoresponse. When the external bias voltages are applied, it can be acted as an OESD and exhibit versatile electrical and photonic synaptic characteristics based on the trapping and detrapping effects, including synaptic plasticity and learning-experience behaviors. More importantly, benefiting from the excellent photosensing ability and transporting properties, the device shows ultralow-power consumption of 39.0 pJ and a 4 × 4 OESDs array is developed to realize the visual perception and memory. This work not only supplies a novel route to realize complex functional integration just in one device, but also offers effective strategies for developing neuromorphic visual system.

Walnut-Derived Peptides Alleviate Learning and Memory Impairments in a Mice Model via Inhibition of Microglia Phagocytose Synapses.

Microglia phagocytose synapses have an important effect on the pathogenesis of neurological disorders. Here, we investigated the neuroprotective effects of the walnut-derived peptide, TWLPLPR(TW-7), against LPS-induced cognitive deficits in mice and explored the underlying C1q-mediated microglia phagocytose synapses mechanisms in LPS-treated HT22 cells. The MWM showed that TW-7 improved the learning and memory capacity of the LPS-injured mice. Both transmission electron microscopy and immunofluorescence analysis illustrated that synaptic density and morphology were increased while associated with the decreased colocalized synapses with C1q. Immunohistochemistry and immunofluorescence demonstrated that TW-7 effectively reduced the microglia phagocytosis of synapses. Subsequently, overexpression of C1q gene plasmid was used to verify the contribution of the TW-7 via the classical complement pathway-regulated mitochondrial function-mediated microglia phagocytose synapses in LPS-treated HT22 cells. These data suggested that TW-7 improved the learning and memory capability of LPS-induced cognitively impaired mice through a mechanism associated with the classical complement pathway-mediated microglia phagocytose synapse.

Equal levels of pre- and postsynaptic potentiation produce unequal outcomes.

Which proportion of the long-term potentiation (LTP) expressed in the bulk of excitatory synapses is postsynaptic and which presynaptic remains debatable. To understand better the possible impact of either LTP form, we explored a realistic model of a CA1 pyramidal cell equipped with known membrane mechanisms and multiple, stochastic excitatory axo-spinous synapses. Our simulations were designed to establish an input-output transfer function, the dependence between the frequency of presynaptic action potentials triggering probabilistic synaptic discharges and the average frequency of postsynaptic spiking. We found that, within the typical physiological range, potentiation of the postsynaptic current results in a greater overall output than an equivalent increase in presynaptic release probability. This difference grows stronger at lower input frequencies and lower release probabilities. Simulations with a non-hierarchical circular network of principal neurons indicated that equal increases in either synaptic fidelity or synaptic strength of individual connections also produce distinct changes in network activity, although the network phenomenology is likely to be complex. These observations should help to interpret the machinery of LTP phenomena documented in situ. This article is part of a discussion meeting issue 'Long-term potentiation: 50 years on'.

Motor Control of Distinct Layer 6 Corticothalamic Feedback Circuits.

Layer 6 corticothalamic (L6 CT) neurons provide massive input to the thalamus, and these feedback connections enable the cortex to influence its own sensory input by modulating thalamic excitability. However, the functional role(s) feedback serves during sensory processing is unclear. One hypothesis is that CT feedback is under the control of extrasensory signals originating from higher-order cortical areas, yet we know nothing about the mechanisms of such control. It is also unclear whether such regulation is specific to CT neurons with distinct thalamic connectivity. Using mice (either sex) combined with in vitro electrophysiology techniques, optogenetics, and retrograde labeling, we describe studies of vibrissal primary motor cortex (vM1) influences on different CT neurons in the vibrissal primary somatosensory cortex (vS1) with distinct intrathalamic axonal projections. We found that vM1 inputs are highly selective, evoking stronger postsynaptic responses in CT neurons projecting to the dual ventral posterior medial nucleus (VPm) and posterior medial nucleus (POm) located in lower L6a than VPm-only-projecting CT cells in upper L6a. A targeted analysis of the specific cells and synapses involved revealed that the greater responsiveness of Dual CT neurons was due to their distinctive intrinsic membrane properties and synaptic mechanisms. These data demonstrate that vS1 has at least two discrete L6 CT subcircuits distinguished by their thalamic projection patterns, intrinsic physiology, and functional connectivity with vM1. Our results also provide insights into how a distinct CT subcircuit may serve specialized roles specific to contextual modulation of tactile-related sensory signals in the somatosensory thalamus during active vibrissa movements.

Superior AlGaN/GaN-Based Phototransistors and Arrays with Reconfigurable Triple-Mode Functionalities Enabled by Voltage-Programmed Two-Dimensional Electron Gas for High-Quality Imaging.

High-quality imaging units are indispensable in modern optoelectronic systems for accurate recognition and processing of optical information. To fulfill massive and complex imaging tasks in the digital age, devices with remarkable photoresponsive characteristics and versatile reconfigurable functions on a single-device platform are in demand but remain challenging to fabricate. Herein, an AlGaN/GaN-based double-heterostructure is reported, incorporated with a unique compositionally graded AlGaN structure to generate a channel of polarization-induced two-dimensional electron gas (2DEGs). Owing to the programmable feature of the 2DEGs by the combined gate and drain voltage inputs, with a particular capability of electron separation, collection and storage under different light illumination, the phototransistor shows reconfigurable multifunctional photoresponsive behaviors with superior characteristics. A self-powered mode with a responsivity over 100 A W-1 and a photoconductive mode with a responsivity of ≈108 A W-1 are achieved, with the ultimate demonstration of a 10 × 10 device array for imaging. More intriguingly, the device can be switched to photoelectric synapse mode, emulating synaptic functions to denoise the imaging process while prolonging the image storage ability. The demonstration of three-in-one operational characteristics in a single device offers a new path toward future integrated and multifunctional imaging units.

Ultrastructural Changes of Synapses in the Hippocampus of Sprague Dawley Rat Brain following Exposure to Naphthalene Balls.

Introduction: The synaptic contacts play an important role in central nervous system (CNS) functioning. Ultrastructural features of synapses in CNS are not studied in naphthalene neurotoxicity model. Materials and Methodology: In the present work, transmission electron microscopy was used for studying the ultrastructural features of synapses in the hippocampus of Sprague Dawley rat brain, on subsequent exposure to naphthalene balls. The ultrastructural changes were observed for naphthalene low dose (200 mg), high dose (400 mg) after the treatment for 28 days, and post-delayed toxicity phase after 14 days in Sprague Dawley rats. Results: In comparison with different groups of naphthalene exposure including control and satellite, axon degeneration, axonal demyelination and abnormal synapses was observed in high dose naphthalene administration group. In the post-delayed naphthalene toxicity group, degeneration of synaptic contacts was observed. Conclusions: This exploration of ultrastructural variations in the synapses of Hippocampus gives information that will be valued in naphthalene neurotoxicological research.

Improved DiOlistic labelling technique for neurons in situ: Detailed visualisation of dendritic spines and concurrent histochemical-detection in fixed tissue.

DiOlistic labelling is a robust, unbiased ballistic method that utilises lipophilic dyes to morphologically label neurons. While its efficacy on freshly dissected tissue specimens is well-documented, applying DiOlistic labelling to stored, fixed brain tissue and its use in polychromatic multi-marker studies poses significant technical challenges. Here, we present an improved, step-by-step protocol for DiOlistic labelling of dendrites and dendritic spines in fixed mouse tissue. Our protocol encompasses the five key stages: Tissue Preparation, Dye Bullet Preparation, DiOlistic Labelling, Confocal Imaging, and Image Analysis. This method ensures reliable and consistent labelling of dendritic spines in fixed mouse tissue, combined with increased throughput of samples and multi-parameter staining and visualisation of tissue, thereby offering a valuable approach for neuroscientific research.

New-Style Logic Operation and Neuromorphic Computing Enabled by Optoelectronic Artificial Synapses in an MXene/Y:HfO2 Ferroelectric Memristor.

Today's computing systems, to meet the enormous demands of information processing, have driven the development of brain-inspired neuromorphic systems. However, there are relatively few optoelectronic devices in most brain-inspired neuromorphic systems that can simultaneously regulate the conductivity through both optical and electrical signals. In this work, the Au/MXene/Y:HfO2/FTO ferroelectric memristor as an optoelectronic artificial synaptic device exhibited both digital and analog resistance switching (RS) behaviors under different voltages with a good switching ratio (>103). Under optoelectronic conditions, optimal weight update parameters and an enhanced algorithm achieved 97.1% recognition accuracy in convolutional neural networks. A new logic gate circuit specifically designed for optoelectronic inputs was established. Furthermore, the device integrates the impact of relative humidity to develop an innovative three-person voting mechanism with a veto power. These results provide a feasible approach for integrating optoelectronic artificial synapses with logic-based computing devices.

In2O3/ZnO heterojunction thin film transistor for high recognition accuracy neuromorphic computing and optoelectronic artificial synapses.

Solid electrolyte-gated transistors exhibit improved chemical stability and can fulfill the requirements of microelectronic packaging. Typically, metal oxide semiconductors are employed as channel materials. However, the extrinsic electron transport properties of these oxides, which are often prone to defects, pose limitations on the overall electrical performance. Achieving excellent repeatability and stability of transistors through the solution process remains a challenging task. In this study, we propose the utilization of a solution-based method to fabricate an In2O3/ZnO heterojunction structure, enabling the development of efficient multifunctional optoelectronic devices. The heterojunction's upper and lower interfaces induce energy band bending, resulting in the accumulation of a large number of electrons and a significant enhancement in transistor mobility. To mimic synaptic plasticity responses to electrical and optical stimuli, we utilize Li+-doped high-k ZrOxthin films as a solid electrolyte in the device. Notably, the heterojunction transistor-based convolutional neural network achieves a high accuracy rate of 93% in recognizing handwritten digits. Moreover, our research involves the simulation of a typical sensory neuron, specifically a nociceptor, within our synaptic transistor. This research offers a novel avenue for the advancement of cost-effective three-terminal thin-film transistors tailored for neuromorphic applications.

Recent advancements in implantable neural links based on organic synaptic transistors.

The progress of brain synaptic devices has witnessed an era of rapid and explosive growth. Because of their integrated storage, excellent plasticity and parallel computing, and system information processing abilities, various field effect transistors have been used to replicate the synapses of a human brain. Organic semiconductors are characterized by simplicity of processing, mechanical flexibility, low cost, biocompatibility, and flexibility, making them the most promising materials for implanted brain synaptic bioelectronics. Despite being used in numerous intelligent integrated circuits and implantable neural linkages with multiple terminals, organic synaptic transistors still face many obstacles that must be overcome to advance their development. A comprehensive review would be an excellent tool in this respect. Therefore, the latest advancements in implantable neural links based on organic synaptic transistors are outlined. First, the distinction between conventional and synaptic transistors are highlighted. Next, the existing implanted organic synaptic transistors and their applicability to the brain as a neural link are summarized. Finally, the potential research directions are discussed.