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1.
Emulation of Synaptic Plasticity on a Cobalt-Based Synaptic Transistor for Neuromorphic Computing.
Monalisha, P, Kumar, APS, Wang, XR, Piramanayagam, SN
ACS applied materials & interfaces. 2022;(9):11864-11872
Abstract
Neuromorphic computing (NC), which emulates neural activities of the human brain, is considered for the low-power implementation of artificial intelligence. Toward realizing NC, fabrication, and investigations of hardware elements─such as synaptic devices and neurons─are crucial. Electrolyte gating has been widely used for conductance modulation by massive carrier injections and has proven to be an effective way of emulating biological synapses. Synaptic devices, in the form of synaptic transistors, have been studied using various materials. Despite the remarkable progress, the study of metallic channel-based synaptic transistors remains massively unexplored. Here, we demonstrated a three-terminal electrolyte gating-modulated synaptic transistor based on a metallic cobalt thin film to emulate biological synapses. We have realized gating-controlled, non-volatile, and distinct multilevel conductance states in the proposed device. The essential synaptic functions demonstrating both short-term and long-term plasticity have been emulated in the synaptic device. A transition from short-term to long-term memory has been realized by tuning the gate pulse parameters, such as amplitude and duration. The crucial cognitive behavior, including learning, forgetting, and re-learning, has been emulated, showing a resemblance to the human brain. Beyond that, dynamic filtering behavior has been experimentally implemented in the synaptic device. These results provide an insight into the design of metallic channel-based synaptic transistors for NC.
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2.
Gut Microbiota and Neuroplasticity.
Murciano-Brea, J, Garcia-Montes, M, Geuna, S, Herrera-Rincon, C
Cells. 2021;(8)
Abstract
The accumulating evidence linking bacteria in the gut and neurons in the brain (the microbiota-gut-brain axis) has led to a paradigm shift in the neurosciences. Understanding the neurobiological mechanisms supporting the relevance of actions mediated by the gut microbiota for brain physiology and neuronal functioning is a key research area. In this review, we discuss the literature showing how the microbiota is emerging as a key regulator of the brain's function and behavior, as increasing amounts of evidence on the importance of the bidirectional communication between the intestinal bacteria and the brain have accumulated. Based on recent discoveries, we suggest that the interaction between diet and the gut microbiota, which might ultimately affect the brain, represents an unprecedented stimulus for conducting new research that links food and mood. We also review the limited work in the clinical arena to date, and we propose novel approaches for deciphering the gut microbiota-brain axis and, eventually, for manipulating this relationship to boost mental wellness.
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3.
Differences in brain structure and theta burst stimulation-induced plasticity implicate the corticomotor system in loss of function after musculoskeletal injury.
Flanagan, SD, Proessl, F, Dunn-Lewis, C, Sterczala, AJ, Connaboy, C, Canino, MC, Beethe, AZ, Eagle, SR, Szivak, TK, Onate, JA, et al
Journal of neurophysiology. 2021;(4):1006-1021
Abstract
Traumatic musculoskeletal injury (MSI) may involve changes in corticomotor structure and function, but direct evidence is needed. To determine the corticomotor basis of MSI, we examined interactions among skeletomotor function, corticospinal excitability, corticomotor structure (cortical thickness and white matter microstructure), and intermittent theta burst stimulation (iTBS)-induced plasticity. Nine women with unilateral anterior cruciate ligament rupture (ACL) 3.2 ± 1.1 yr prior to the study and 11 matched controls (CON) completed an MRI session followed by an offline plasticity-probing protocol using a randomized, sham-controlled, double-blind, cross-over study design. iTBS was applied to the injured (ACL) or nondominant (CON) motor cortex leg representation (M1LEG) with plasticity assessed based on changes in skeletomotor function and corticospinal excitability compared with sham iTBS. The results showed persistent loss of function in the injured quadriceps, compensatory adaptations in the uninjured quadriceps and both hamstrings, and injury-specific increases in corticospinal excitability. Injury was associated with lateralized reductions in paracentral lobule thickness, greater centrality of nonleg corticomotor regions, and increased primary somatosensory cortex leg area inefficiency and eccentricity. Individual responses to iTBS were consistent with the principles of homeostatic metaplasticity; corresponded to injury-related differences in skeletomotor function, corticospinal excitability, and corticomotor structure; and suggested that corticomotor adaptations involve both hemispheres. Moreover, iTBS normalized skeletomotor function and corticospinal excitability in ACL. The results of this investigation directly confirm corticomotor involvement in chronic loss of function after traumatic MSI, emphasize the sensitivity of the corticomotor system to skeletomotor events and behaviors, and raise the possibility that brain-targeted therapies could improve recovery.NEW & NOTEWORTHY Traumatic musculoskeletal injuries may involve adaptive changes in the brain that contribute to loss of function. Our combination of neuroimaging and theta burst transcranial magnetic stimulation (iTBS) revealed distinct patterns of iTBS-induced plasticity that normalized differences in muscle and brain function evident years after unilateral knee ligament rupture. Individual responses to iTBS corresponded to injury-specific differences in brain structure and physiological activity, depended on skeletomotor deficit severity, and suggested that corticomotor adaptations involve both hemispheres.
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4.
White matter plasticity in healthy older adults: The effects of aerobic exercise.
Mendez Colmenares, A, Voss, MW, Fanning, J, Salerno, EA, Gothe, NP, Thomas, ML, McAuley, E, Kramer, AF, Burzynska, AZ
NeuroImage. 2021;:118305
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Abstract
White matter deterioration is associated with cognitive impairment in healthy aging and Alzheimer's disease. It is critical to identify interventions that can slow down white matter deterioration. So far, clinical trials have failed to demonstrate the benefits of aerobic exercise on the adult white matter using diffusion Magnetic Resonance Imaging. Here, we report the effects of a 6-month aerobic walking and dance interventions (clinical trial NCT01472744) on white matter integrity in healthy older adults (n = 180, 60-79 years) measured by changes in the ratio of calibrated T1- to T2-weighted images (T1w/T2w). Specifically, the aerobic walking and social dance interventions resulted in positive changes in the T1w/T2w signal in late-myelinating regions, as compared to widespread decreases in the T1w/T2w signal in the active control. Notably, in the aerobic walking group, positive change in the T1w/T2w signal correlated with improved episodic memory performance. Lastly, intervention-induced increases in cardiorespiratory fitness did not correlate with change in the T1w/T2w signal. Together, our findings suggest that white matter regions that are vulnerable to aging retain some degree of plasticity that can be induced by aerobic exercise training. In addition, we provided evidence that the T1w/T2w signal may be a useful and broadly accessible measure for studying short-term within-person plasticity and deterioration in the adult human white matter.
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5.
Energy sensors in drug addiction: A potential therapeutic target.
López-Gambero, AJ, Rodríguez de Fonseca, F, Suárez, J
Addiction biology. 2021;(2):e12936
Abstract
Addiction is defined as the repeated exposure and compulsive seek of psychotropic drugs that, despite the harmful effects, generate relapse after the abstinence period. The psychophysiological processes associated with drug addiction (acquisition/expression, withdrawal, and relapse) imply important alterations in neurotransmission and changes in presynaptic and postsynaptic plasticity and cellular structure (neuroadaptations) in neurons of the reward circuits (dopaminergic neuronal activity) and other corticolimbic regions. These neuroadaptation mechanisms imply important changes in neuronal energy balance and protein synthesis machinery. Scientific literature links drug-induced stimulation of dopaminergic and glutamatergic pathways along with presence of neurotrophic factors with alterations in synaptic plasticity and membrane excitability driven by metabolic sensors. Here, we provide current knowledge of the role of molecular targets that constitute true metabolic/energy sensors such as AMPK, mTOR, ERK, or KATP in the development of the different phases of addiction standing out the main brain regions (ventral tegmental area, nucleus accumbens, hippocampus, and amygdala) constituting the hubs in the development of addiction. Because the available treatments show very limited effectiveness, evaluating the drug efficacy of AMPK and mTOR specific modulators opens up the possibility of testing novel pharmacotherapies for an individualized approach in drug abuse.
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6.
Optimizing Chronic Pain Treatment with Enhanced Neuroplastic Responsiveness: A Pilot Randomized Controlled Trial.
Pratscher, S, Mickle, AM, Marks, JG, Rocha, H, Bartsch, F, Schmidt, J, Tejera, L, Garcia, S, Custodero, C, Jean, F, et al
Nutrients. 2021;(5)
Abstract
Chronic pain affects mental and physical health and alters brain structure and function. Interventions that reduce chronic pain are also associated with changes in the brain. A number of non-invasive strategies can promote improved learning and memory and increase neuroplasticity in older adults. Intermittent fasting and glucose administration represent two such strategies with the potential to optimize the neurobiological environment to increase responsiveness to recognized pain treatments. The purpose of the pilot study was to test the feasibility and acceptability of intermittent fasting and glucose administration paired with a recognized pain treatment activity, relaxation and guided imagery. A total of 32 adults (44% W, 56% M), 50 to 85 years of age, with chronic knee pain for three months or greater participated in the study. Four sessions were completed over an approximate two-week period. Findings indicate the ability to recruit, randomize, and retain participants in the protocol. The procedures and measures were reasonable and completed without incident. Participant adherence was high and exit interview feedback positive. In summary, the pilot study was feasible and acceptable, providing the evidence necessary to move forward with a larger clinical trial.
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7.
Determination of anodal tDCS duration threshold for reversal of corticospinal excitability: An investigation for induction of counter-regulatory mechanisms.
Hassanzahraee, M, Nitsche, MA, Zoghi, M, Jaberzadeh, S
Brain stimulation. 2020;(3):832-839
Abstract
BACKGROUND Transcranial direct current stimulation (tDCS) is used to induce neuroplasticity in the human brain. Within certain limits of stimulation duration, anodal tDCS (a-tDCS) over the primary motor cortex induces long term potentiation- (LTP) like plasticity. A reversal of the direction of plasticity has however been described with prolonged a-tDCS protocols. OBJECTIVE We aimed to systematically investigate the intervention duration threshold for reversal of a-tDCS-induced effects on corticospinal excitability (CSE) and to determine the probable mechanisms involved in these changes. METHODS Fifteen healthy participants received a-tDCS of 1 mA for five different durations in pseudo-random session order. Transcranial magnetic stimulation (TMS) was delivered over the left M1, and motor evoked potentials (MEPs) of a contralateral hand muscle were recorded before, immediately and 30 min following intervention to measure CSE changes. Short-interval intracortical inhibition (SICI), intracortical facilitation (ICF), and long interval facilitation (LIF) were assessed via paired-pulse TMS protocols. RESULTS A-tDCS significantly increased CSE as expected at stimulation durations of 22 and 24 min. However, this effect of a-tDCS on CSE decreased and even reversed when stimulation duration increased to 26, 28, and 30 min. Respective alterations of ICF, LIF, and SICI indicate the involvement of glutamatergic, and GABAergic systems in these effects. CONCLUSIONS These results confirm a duration threshold for reversal of the excitability-enhancing effect of a-tDCS with stimulation durations ≥ 26 min. Counter-regulatory mechanisms are discussed as a mechanistic foundation for these effects, which might prevent excessive brain activation.
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8.
Vitamin A: its many roles-from vision and synaptic plasticity to infant mortality.
Dowling, JE
Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology. 2020;(3):389-399
Abstract
The recognition that a dietary factor is essential to maintain good and sensitive vision as well as overall health goes back over 3,000 years to the ancient Egyptians. With the discovery of the vitamins at the turn of the twentieth century, fat-soluble vitamin A was soon shown to be the essential factor. In the first half of the twentieth century, the role vitamin A plays in vision, as precursor to the light-sensitive visual pigment molecules in the photoreceptors was elegantly worked out, especially by George Wald and his colleagues. Beginning in the 1960s, with the recognition of the active metabolite of vitamin A, its acid form now called retinoic acid, the roles of vitamin A in maintaining overall health of an organism began to be explored, and this research continues to this day. Receptors activated by retinoic acid, the RARs and RXRs have been shown to regulate gene transcription in a surprisingly wide variety of biological processes from early growth and development to the maintenance of epithelial tissues in many organs, the regulation of the immune system, and even the modulation of synaptic function in the brain involved in mechanisms underlying memory and learning. Therapeutic uses for retinoic acid have been developed, including one for a specific form of leukemia. The story is by no means complete and it is likely more surprises await with regard to this remarkable molecule.
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9.
Actomyosin Contractility in the Generation and Plasticity of Axons and Dendritic Spines.
Mikhaylova, M, Rentsch, J, Ewers, H
Cells. 2020;(9)
Abstract
Actin and non-muscle myosins have long been known to play important roles in growth cone steering and neurite outgrowth. More recently, novel functions for non-muscle myosin have been described in axons and dendritic spines. Consequently, possible roles of actomyosin contraction in organizing and maintaining structural properties of dendritic spines, the size and location of axon initial segment and axonal diameter are emerging research topics. In this review, we aim to summarize recent findings involving myosin localization and function in these compartments and to discuss possible roles for actomyosin in their function and the signaling pathways that control them.
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10.
A calcium-influx-dependent plasticity model exhibiting multiple STDP curves.
Houben, AM, Keil, MS
Journal of computational neuroscience. 2020;(1):65-84
Abstract
Hebbian plasticity means that if the firing of two neurons is correlated, then their connection is strengthened. Conversely, uncorrelated firing causes a decrease in synaptic strength. Spike-timing-dependent plasticity (STDP) represents one instantiation of Hebbian plasticity. Under STDP, synaptic changes depend on the relative timing of the pre- and post-synaptic firing. By inducing pre- and post-synaptic firing at different relative times the STDP curves of many neurons have been determined, and it has been found that there are different curves for different neuron types or synaptic sites. Biophysically, strengthening (long-term potentiation, LTP) or weakening (long-term depression, LTD) of glutamatergic synapses depends on the post-synaptic influx of calcium (Ca2+): weak influx leads to LTD, while strong, transient influx causes LTP. The voltage-dependent NMDA receptors are the main source of Ca2+ influx, but they will only open if a post-synaptic depolarisation coincides with pre-synaptic neurotransmitter release. Here we present a computational mechanism for Ca2+-dependent plasticity in which the interplay between the pre-synaptic neurotransmitter release and the post-synaptic membrane potential leads to distinct Ca2+ time-courses, which in turn lead to the change in synaptic strength. It is shown that the model complies with classic STDP results, as well as with results obtained with triplets of spikes. Furthermore, the model is capable of displaying different shapes of STDP curves, as observed in different experimental studies.