Neural Circuits Research Articles

Social neuroscience: When more is merrier

Spiny mice are gregarious animals that prefer to socialize with large groups. A new pioneering study reveals an underlying neural circuit governing this social preference.

Mechanistic insight of neurodegeneration due to micro/nano-plastic-induced gut dysbiosis.

Despite offering significant conveniences, plastic materials contribute substantially in developing environmental hazards and pollutants. Plastic trash that has not been adequately managed may eventually break down into fragments caused by human or ecological factors. Arguably, the crucial element for determining the biological toxicities of plastics are micro/nano-forms ofplastics (MPs/NPs), which infiltrate the mammalian tissue through different mediaand routes. Infiltration of MPs/NPs across the intestinal barrier leads to microbial architectural dysfunction, which further modulates the population of gastrointestinal microbes. Thereby, it triggers inflammatory mediators (e.g., IL-1α/β, TNF-α, and IFN-γ) by activating specific receptors located in the gut barrier. Mounting evidence indicates that MPs/NPs disrupt host pathophysiological function through modification of junctional proteins and effector cells. Moreover, the alteration of microbial diversity by MPs/NPs causes the breakdown of the blood-brain barrier and translocation of metabolites (e.g., SCFAs, LPS) through the vagus nerve. Potent penetration affects the neuronal networks, neuronal protein accumulation, acceleration of oxidative stress, and alteration of neurofibrillary tangles, and hinders distinctive communicatingpathways. Conclusively, alterations of these neurotoxic factors are possibly responsible forthe associated neurodegenerative disordersdue to the exposure of MPs/NPs. In this review, the hypothesis on MPs/NPs associated with gut microbial dysbiosis has been interlinked to the distinct neurological impairment through the gut-brain axis.

12237 Monosynaptic Gabaergic Signaling From Suprachiasmatic Nucleus Neuromedin S Neurons To Preoptic Area Kisspeptin Neurons In Mice

Abstract Disclosure: W.I. Abdulmajeed: None. B.B. Jamieson: None. S.X. Thomas: None. Y. Rim: None. A.G. Novak: None. R.E. Campbell: None. R. Piet: None. In female rodents, projections from suprachiasmatic nucleus (SCN) neurons relay timing cues to the gonadotropin-releasing hormone (GnRH) neuronal network for the preovulatory surge. Kisspeptin (KISS1) neurons of the rostral periventricular area of the third ventricle (RP3V) are thought to integrate these cues with estradiol positive feedback to drive GnRH neuron activity, the gonadotropin surge and ovulation. We recently reported that SCN neuron projections release arginine vasopressin (AVP), thereby stimulating female RP3VKiss[1] neuron action potential firing in an estrous cycle stage-dependent manner. In the SCN, AVP is expressed in a subset of neuromedin S (NMS) neurons, a neuronal population essential for circadian rhythms. Moreover, a previous report indicates that exogenous NMS stimulates LH secretion in female rodents. SCNNMS neurons might, therefore, play a role in timing the preovulatory surge. However, whether SCNNMS neurons project to and regulate the activity of RP3VKISS[1] neurons is currently unknown. To address this question, we combined anterograde viral tract-tracing and channelrhodopsin-2 (ChR2)- assisted circuit mapping. Female mice expressing Cre recombinase in NMS cells (NMS-Cre) received stereotaxic injections in the SCN of adeno-associated viral vectors (AAVs) carrying the Cre-dependent sequence for mCherry. Fluorescence immunohistochemistry revealed that mCherry-expressing fibers come in close apposition with the great majority (>80%) of KISS1-immunoreactive neurons in the RP3V, suggesting a SCNNMS-to-RP3VKISS[1] neuron circuit. To interrogate this circuit, we next injected AAVs carrying Cre-dependent channelrhodopsin (ChR2) in the SCN of female NMS-Cre mice that also express the green fluorescent protein in KISS1 cells. Blue LED light (460-487 nm) activation of ChR2-expressing SCNNMS neuronal fibers in the RP3V evoked postsynaptic currents (PSCs) in most KISS1 neurons recorded in whole-cell voltage clamp (-60 mV) in brain slices. Evoked PSCs had short latencies and were blocked by bath application of 0.5 µM tetrodotoxin (TTX), indicating that they were generated by action potential-dependent release. Addition of 100 µM 4-Aminopyridine (4-AP, a potassium channel blocker) to TTX rescued these responses, indicating the existence of a monosynaptic SCNNMS-to-RP3VKISS[1] connection. In addition, evoked PSCs were suppressed by 5 µM gabazine, a GABAA receptor antagonist, but not by 20 µM NBQX and 50 µM D-AP5, AMPA- and NMDA-type glutamate receptor antagonists, respectively, revealing that SCNNMS projections release GABA onto RP3VKISS[1] neurons. Together, our findings are consistent with SCNNMS neurons extending monosynaptic GABAergic projections to RP3VKISS[1] neurons. Further studies are needed to determine the impact of these projections on RP3VKISS[1] neuron activity and the role they might play in the preovulatory surge. Presentation: 6/1/2024

7170 Plasticity of the Hypothalamic Tuberoinfundibular Dopaminergic Neuronal Network in Lactating Rats

Abstract Disclosure: P. Papaioannou: None. T. Georgescu: None. D.R. Grattan: None. S. Bunn: None. S. Yip: None. The tuberoinfundibular dopaminergic (TIDA) neurons play a crucial role in regulating prolactin secretion. Their synchronized network activity with slow but highly rhythmic firing pattern is important for dopamine release in rats[1]. While this unique TIDA network activity is vital for prolactin negative feedback in non-lactating conditions, its behaviour during lactation, when prolactin demand is high, remains unknown. Our hypothesis posited that the TIDA neuronal network in lactating rats becomes desynchronized, disrupting the negative feedback loop. To test this, we utilized ex-vivo Ca2+ imaging to simultaneously monitor population-wide TIDA neuron activity in non-lactating (NL; n=13) and lactating (L; n=10) rats injected with a cre-inducible adeno-associated virus (AAV) containing the Ca2+ indicator, GCaMP6s, into their arcuate nucleus. Analysis of neuronal network synchronicity revealed significant desynchronization in the TIDA network during lactation, as indicated by a markedly lower mean correlation coefficient matrix (CM) compared to non-lactating conditions (NL: 0.87±0.02, n= 26 sections vs L: 0.22±0.03, n=29 sections; p<0.001, Student’s t-test). Furthermore, the oscillatory activity patterns of these desynchronized TIDA neurons displayed a significantly lower cell rhythmicity index (RI) in lactating animals compared to non-lactating ones (NL: 0.17±0.01, n=186 cells vs L: 0.70±0.02, n=77 cells; p<0.001, Student’s t-test). Interestingly, within these low rhythmic neurons, some exhibited higher while others showed lower firing frequencies compared to non-lactating TIDA neurons. After 7 days post-weaning (n=4 animals), the TIDA network activity returned to non-lactating behaviour (CM = 0.85 ± 0.04, n=6 sections and RI = 0.17±0.01; n=47 cells). In summary, our findings demonstrate a reversible reconfiguration of the TIDA neuronal networks during lactation, characterized by low rhythmic oscillations and individual unique firing patterns, leading to diminished intercellular synchrony that may impede dopamine release, ultimately facilitating prolactin release to support lactation. Once weaned, the TIDA neuronal network reset to NL state to allow a new reproductive cycle. [1] Lyons, D. J., Horjales-Araujo, E. & Broberger, C. Synchronized network oscillations in rat tuberoinfundibular dopamine neurons: switch to tonic discharge by thyrotropin-releasing hormone. Neuron 65, 217-229, doi:10.1016/j.neuron.2009.12.024 (2010). Presentation: 6/2/2024

9271 Cholinergic Signaling in the Mouse Embryonic Pancreas Targets Early Endocrine Cells

Abstract Disclosure: C. Duarte: None. J.K. Panzer: None. N. Borowsky: None. A. Caicedo: None. The parasympathetic vagus nerve affects pancreas function by activating local intrapancreatic neurons that release acetylcholine (ACh). These neurons are derived from progenitors of the vagal neural crest and colonize the pancreas during embryonic development. The specific mechanisms by which ACh is released from these neurons influence embryonic development of the islet and, specifically, beta cells remain largely unknown. The purpose of this study was to identify cholinergic signaling components and assess early physiological responses to ACh during murine development of endocrine lineage cells. We extracted pancreatic rudiments from mice at embryonic stages E15 to E18 and stained them for neuronal and endocrine markers, along with components associated with cholinergic signaling. We further performed Ca2+ imaging of the pancreatic rudiments from NGN3CRE-GCaMP3 mice to record responses to ACh in cells of the endocrine lineage. At E15, we observed a significantly higher concentration of glucagon+ cells compared to insulin+ cells, consistent with the earlier differentiation of alpha cells in the developing pancreas. Neuronal body clusters were identified in close proximity to endocrine lineage cells from E15 to E18, with the neuronal network becoming more dispersed and interconnected. At E15, wide distribution of the presynaptic vesicular acetylcholine transporter (VAChT) was observed later becoming localized around insulin+ and glucagon+ cells at E18. Postsynaptic acetylcholinesterase (AChE) colocalized with glucagon+ cells from E15 to E18 and with insulin+ cells by E18. ACh elicited Ca2+ responses in individual endocrine cells as early as E15. Our results show that cholinergic nerve terminals target early endocrine cells and elicit responses to ACh, indicating that local cholinergic neurons innervate and activate endocrine progenitors in the embryonic pancreas. Our current studies are aimed at determining how cholinergic signaling contributes to beta cell differentiation and function. We expect this knowledge to guide future protocols for deriving beta cells from stem cells. Presentation: 6/2/2024

8715 Cholinergic Signaling in the Mouse Embryonic Pancreas Targets Early Endocrine Cells

Abstract Disclosure: C. Duarte: None. J.K. Panzer: None. N. Borowsky: None. A. Caicedo: None. The parasympathetic vagus nerve affects pancreas function by activating local intrapancreatic neurons that release acetylcholine (ACh). These neurons are derived from progenitors of the vagal neural crest and colonize the pancreas during embryonic development. The specific mechanisms by which ACh is released from these neurons influence embryonic development of the islet and, specifically, beta cells remain largely unknown. The purpose of this study was to identify cholinergic signaling components and assess early physiological responses to ACh during murine development of endocrine lineage cells. We extracted pancreatic rudiments from mice at embryonic stages E15 to E18 and stained them for neuronal and endocrine markers, along with components associated with cholinergic signaling. We further performed Ca2+ imaging of the pancreatic rudiments from NGN3CRE-GCaMP3 mice to record responses to ACh in cells of the endocrine lineage. At E15, we observed a significantly higher concentration of glucagon+ cells compared to insulin+ cells, consistent with the earlier differentiation of alpha cells in the developing pancreas. Neuronal body clusters were identified in close proximity to endocrine lineage cells from E15 to E18, with the neuronal network becoming more dispersed and interconnected. At E15, wide distribution of the presynaptic vesicular acetylcholine transporter (VAChT) was observed later becoming localized around insulin+ and glucagon+ cells at E18. Postsynaptic acetylcholinesterase (AChE) colocalized with glucagon+ cells from E15 to E18 and with insulin+ cells by E18. ACh elicited Ca2+ responses in individual endocrine cells as early as E15. Our results show that cholinergic nerve terminals target early endocrine cells and elicit responses to ACh, indicating that local cholinergic neurons innervate and activate endocrine progenitors in the embryonic pancreas. Our current studies are aimed at determining how cholinergic signaling contributes to beta cell differentiation and function. We expect this knowledge to guide future protocols for deriving beta cells from stem cells. Presentation: 6/2/2024

Multifunctional human visual pathway-replicated hardware based on 2D materials

Artificial visual system empowered by 2D materials-based hardware simulates the functionalities of the human visual system, leading the forefront of artificial intelligence vision. However, retina-mimicked hardware that has not yet fully emulated the neural circuits of visual pathways is restricted from realizing more complex and special functions. In this work, we proposed a human visual pathway-replicated hardware that consists of crossbar arrays with split floating gate 2D tungsten diselenide (WSe2) unit devices that simulate the retina and visual cortex, and related connective peripheral circuits that replicate connectomics between the retina and visual cortex. This hardware experimentally displays advanced multi-functions of red–green color-blindness processing, low-power shape recognition, and self-driven motion tracking, promoting the development of machine vision, driverless technology, brain–computer interfaces, and intelligent robotics.

Terminal differentiation precedes functional circuit integration in the peduncle neurons in regenerating Hydra vulgaris

Understanding how neural circuits are regenerated following injury is a fundamental question in neuroscience. Hydra is a powerful model for studying this process because it has a simple neural circuit structure, significant and reproducible regenerative abilities, and established methods for creating transgenics with cell-type-specific expression. While Hydra is a long-standing model for regeneration and development, little is known about how neural activity and behavior is restored following significant injury. In this study, we ask if regenerating neurons terminally differentiate prior to reforming functional neural circuits, or if neural circuits regenerate first and then guide the constituent naive cells toward their terminal fate. To address this question, we developed a dual-expression transgenic Hydra line that expresses a cell-type-specific red fluorescent protein (tdTomato) in ec5 peduncle neurons, and a calcium indicator (GCaMP7s) in all neurons. With this transgenic line, we can simultaneously record neural activity and track the reappearance of the terminally-differentiated ec5 neurons. Using SCAPE (Swept Confocally Aligned Planar Excitation) microscopy, we monitored both calcium activity and expression of tdTomato-positive neurons in 3D with single-cell resolution during regeneration of Hydra’s aboral end. The synchronized neural activity associated with a regenerated neural circuit was observed approximately 4 to 8 hours after expression of tdTomato in ec5 neurons. These data suggest that regenerating ec5 neurons undergo terminal differentiation prior to re-establishing their functional role in the nervous system. The combination of dynamic imaging of neural activity and gene expression during regeneration make Hydra a powerful model system for understanding the key molecular and functional processes involved in neural regeneration following injury.

Distinct visual processing networks for foveal and peripheral visual fields

Foveal and peripheral vision are two distinct modes of visual processing essential for navigating the world. However, it remains unclear if they engage different neural mechanisms and circuits within the visual attentional system. Here, we trained macaques to perform a free-gaze visual search task using natural face and object stimuli and recorded a large number of 14588 visually responsive units from a broadly distributed network of brain regions involved in visual attentional processing. Foveal and peripheral units had substantially different proportions across brain regions and exhibited systematic differences in encoding visual information and visual attention. The spike-local field potential (LFP) coherence of foveal units was more extensively modulated by both attention and visual selectivity, thus indicating differential engagement of the attention and visual coding network compared to peripheral units. Furthermore, we delineated the interaction and coordination between foveal and peripheral processing for spatial attention and saccade selection. Together, the systematic differences between foveal and peripheral processing provide valuable insights into how the brain processes and integrates visual information from different regions of the visual field.

Extended human agency: towards a teleological account of AI

This paper analyzes human-machine interrelation concerning artificial neuronal networks (ANNs) from a teleological point of view. The paper argues that AI cannot be understood adequately in terms of subjectivity or objectivity but rather as a new kind of teleological relationship that holds between human and artificial performances of intelligence. Thereby, AI is understood as an enactivist extension of human agency, both in instrumental and moral terms. This hybrid account will be distinguished from four alternative accounts of human-machine relations: (i) the simulation account, according to which AI simulates human rationality; (ii) the instrumentalist account, according to which AI is just a tool; (iii) the anthropomorphic account, according to which AI is human-like; and (iv) the indifference account, according to which AI will merge with human rationality due to technological progress. Against these four accounts, the paper argues for a teleological account of AI as extended human agency that is part of the human lifeworld. By focusing on the teleological interrelation of socially grounded databases and algorithms, the paper finally develops an account of responsible AI that considers its specific relatedness with human actions, purposes, and intentions by means of language. Understanding human-machine relations in terms of extended agency finally allows to tackle the question of how to avoid the problems of AI bias and opacity.

Harnessing brain-body communication to understand cancer.

Solid tumors that arise in the body interact with neurons, which influences cancer progression and treatment response. Here, we discuss key questions in the field, including defining the nature of interactions between tumors and neural circuits and defining how neural signals shape the tumor microenvironment. This information will allow us to optimally target neural signaling to improve outcomes for cancer patients.

Simulating the motion of a mechanical arm driven by neural circuit

A simple electromechanical model is constructed in this work to investigate the dynamical behavior of a mechanical arm driven by a light-sensitive neural circuit, simulating the operation of a micromechanical device implanted in the brain under neuronal operation. The physical equation describing the relationship between neural firing and mechanical motion is provided, the dimensionless model is obtained using the scale transformation, and the Hamilton energy of the electromechanical system is calculated based on Helmholtz theorem. It is found that the variation of photocurrent, magnetic field and damping coefficient causes the neuron and mechanical arm to interact with each other to generate a variety of oscillations when the phototube is used as a voltage/current source. Furthermore, it is demonstrated that the conversion of field energy and mechanical energy is another effective method for estimating and controlling the oscillation modes of the electromechanical model. The results explain how a micromassager connected to a neuron processes information from both environment and itself, and provide an insight for the design of implantable neurostimulators to restore brain or muscle function.

What a wonderful world!

The world of cancer science is moving toward a paradigm shift in making connections with neuroscience. After decades of research on genetic instability and mutations or on the tumor microenvironment, emerging evidence suggests that a malignant tumor is able to hijack and use the brain and its network of peripheral and central neurons as disrupters of homeostasis in the body. Whole-body homeostasis requires brain-body circuits to maintain survival and health via the processes of interoception, immunoception, and nociception. It is now likely that cancer disturbs physiological brain-body communication in making bidirectional brain tumor connections.

Maintaining and updating accurate internal representations of continuous variables with a handful of neurons.

Many animals rely on persistent internal representations of continuous variables for working memory, navigation, and motor control. Existing theories typically assume that large networks of neurons are required to maintain such representations accurately; networks with few neurons are thought to generate discrete representations. However, analysis of two-photon calcium imaging data from tethered flies walking in darkness suggests that their small head-direction system can maintain a surprisingly continuous and accurate representation. We thus ask whether it is possible for a small network to generate a continuous, rather than discrete, representation of such a variable. We show analytically that even very small networks can be tuned to maintain continuous internal representations, but this comes at the cost of sensitivity to noise and variations in tuning. This work expands the computational repertoire of small networks, and raises the possibility that larger networks could represent more and higher-dimensional variables than previously thought.

Deciphering visceral instincts: a scientific quest to unravel food choices from molecules to mind.

The study of biological mechanisms, while crucial, cannot fully explain complex phenomena like the instinct to eat. The mind-body connection, as exemplified by the concept of "voodoo death," highlights the profound influence of belief and cultural context on physiology. Indigenous knowledge systems further emphasize the interconnectedness of humans with their environment. Recent discoveries in gut-brain communication reveal the intricate neural circuits that drive our visceral desires, but a holistic approach that integrates both physiological mechanisms and the subjective experience of life, informed by diverse cultural perspectives, will be essential to truly understand what it means to be alive.

High-confidence and high-throughput quantification of synapse engulfment by oligodendrocyte precursor cells.

Oligodendrocyte precursor cells (OPCs) sculpt neural circuits through the phagocytic engulfment of synapses during development and adulthood. However, existing techniques for analyzing synapse engulfment by OPCs have limited accuracy. Here we describe the quantification of synapse engulfment by OPCs via a two-pronged cell biological approach that combines high-confidence and high-throughput methodologies. Firstly, an adeno-associated virus encoding a pH-sensitive, fluorescently tagged synaptic marker is expressed in neurons in vivo to differentially label presynaptic inputs, depending upon whether they are outside of or within acidic phagolysosomal compartments. When paired with immunostaining for OPC markers in lightly fixed tissue, this approach quantifies the engulfment of synapses by around 30-50 OPCs in each experiment. The second method uses OPCs isolated from dissociated brain tissue that are then fixed, incubated with fluorescent antibodies against presynaptic proteins, and analyzed by flow cytometry, enabling the quantification of presynaptic material within tens of thousands of OPCs in <1 week. The integration of both methods extends the current imaging-based assays, originally designed to quantify synaptic phagocytosis by other brain cells such as microglia and astrocytes, by enabling the quantification of synaptic engulfment by OPCs at individual and populational levels. With minor modifications, these approaches can be adapted to study synaptic phagocytosis by numerous glial cell types in the brain. The protocol is suitable for users with expertise in both confocal microscopy and flow cytometry. The imaging-based and flow cytometry-based protocols require 5 weeks and 2 d to complete, respectively.

A circuit from lateral hypothalamic to dorsal hippocampal dentate gyrus modulates behavioral despair in mice.

Behavioral despair is one of the clinical manifestations of major depressive disorder and an important cause of disability and death. However, the neural circuit mechanisms underlying behavioral despair are poorly understood. In a well-established chronic behavioral despair (CBD) mouse model, using a combination of viral tracing, in vivo fiber photometry, chemogenetic and optogenetic manipulations, in vitro electrophysiology, pharmacological profiling techniques, and behavioral tests, we investigated the neural circuit mechanisms in regulating behavioral despair. Here, we found that CBD enhanced CaMKIIα neuronal excitability in the dorsal dentate gyrus (dDG) and dDGCaMKIIα neurons involved in regulating behavioral despair in CBD mice. Besides, dDGCaMKIIα neurons received 5-HT inputs from median raphe nucleus (MRN) and were mediated by 5-HT1A receptors, whereas MRN5-HT neurons received CaMKIIα inputs from lateral hypothalamic (LH) and were mediated by AMPA receptors to regulate behavioral despair. Furthermore, fluvoxamine exerted its role in resisting behavioral despair through the LH-MRN-dDG circuit. These findings suggest that a previously unidentified circuit of LHCaMKIIα-MRN5-HT-dDGCaMKIIα mediates behavioral despair induced by CBD. Furthermore, these support the important role of AMPA receptors in MRN and 5-HT1A receptors in dDG that might be the potential targets for treatment of behavioral despair, and explain the neural circuit mechanism of fluvoxamine-resistant behavioral despair.

Beyond pain privacy and pain meters: a new vision for pain biomarkers.

To an individual, pain is unambiguously real. To a caregiver, assessing pain in others is a challenging process shrouded in doubt. To explain this challenge, many assume that pain "belongs" exclusively to the bearer of that experience and accept the dogma that pain is private. However, privacy also entails that it is not possible to identify, share, or communicate that experience with others. Obviously, this is not true and the consequences of pain privacy would be devastating for healthcare. Pain is indeed unique and subjective, but not necessarily private. Pain is in fact readily communicable, though perhaps not as effectively and reliably as caregivers would like. On the other hand, healthcare systems mandate objective metrics in pain diagnosis. Smiley face caricatures are a staple of clinical practice and a universal standard for reporting pain levels. These conditions create a double paradox: Assess a private experience that is inaccessible, and use numerical scales to measure subjective attributes. Navigating this stressful environment, medical professionals experience intellectual dissonance, patients are frustrated, and value-based care is undermined. Offering a way out, first, we refute the privacy and objectification of pain citing philosophical, behavioral, and neuroscientific arguments. We discuss Wittgensteinian views against privacy, explore the clear evolutionary advantage of communicating pain to others, and identify neural circuits in the mammalian brain that contribute to empathy. Second, we highlight the subjectivity of pain, embracing the complexity and uniqueness of an individual's pain. We also provide compelling evidence for brain mechanisms that actively shape the pain experience according to predictive coding principles. Third, we offer a vision for the development of biomarker technologies that assess pain fairly without engendering bias against the patient's narrative. Our recommendations are based on the overwhelming appreciation that "medicine by emoji" is inadequate for capturing the multidimensional nature of pain. Our view is that the most promising candidates for pain biomarkers consist of self-reports as ground truth augmented by physiological signatures of biological relevance to pain. Integration of subjective and objective multimodal features will be key for the development of comprehensive pain assessment models.

Aberrant individual large-scale functional network connectivity and topology in chronic insomnia disorder with and without depression

Insomnia is increasingly prevalent with significant associations with depression. Delineating specific neural circuits for chronic insomnia disorder (CID) with and without depressive symptoms is fundamental to develop precision diagnosis and treatment. In this study, we examine static, dynamic and network topology changes of individual large-scale functional network for CID with (CID-D) and without depression to reveal their specific neural underpinnings. Seventeen individual-specific functional brain networks are obtained using a regularized nonnegative matrix factorization technique. Disorders-shared and -specific differences in static and dynamic large-scale functional network connectivities within or between the cognitive control network, dorsal attention network, visual network, limbic network, and default mode network are found for CID and CID-D. Additionally, CID and CID-D groups showed compromised network topological architecture including reduced small-world properties, clustering coefficients and modularity indicating decreased network efficiency and impaired functional segregation. Moreover, the altered neuroimaging indices show significant associations with clinical manifestations and could serve as effective neuromarkers to distinguish among healthy controls, CID and CID-D. Taken together, these findings provide novel insights into the neural basis of CID and CID-D, which may facilitate developing new diagnostic and therapeutic approaches.

Hysteresis and self-oscillations in an artificial memristive quantum neuron

We theoretically study an artificial neuron circuit containing a quantum memristor in the presence of relaxation and dephasing. The charge transport in the quantum element is realized via tunneling of a charge through a quantum particle which shuttles between two terminals—a functionality reminiscent of classical diffusive memristors. We demonstrate that this physical principle enables hysteretic behavior in the current-voltage characteristics of the quantum device. In addition, being used in an artificial neural circuit, the quantum switcher is able to generate self-sustained current oscillations. Our analysis reveals that these self-oscillations are triggered only in quantum regimes with a moderate rate of relaxation, and cannot exist either in a purely coherent regime or at a very high decoherence. We investigate the hysteresis and instability leading to the onset of current self-oscillations and analyze their properties depending on the circuit parameters. Our results provide a generic approach to the use of quantum regimes for controlling hysteresis and generating self-oscillations. Published by the American Physical Society 2024