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The exponential time differencing (ETD) method allows using a large time step to efficiently evolve stiff systems such as Hodgkin-Huxley (HH) neural networks. For pulse-coupled HH networks, the synaptic spike times cannot be predetermined and are convoluted with neuron's trajectory itself. This presents a challenging issue for the design of an efficient numerical simulation algorithm. The stiffness in the HH equations are quite different, for example, between the spike and non-spike regions. Here, we design a second-order adaptive exponential time differencing algorithm (AETD2) for the numerical evolution of HH neural networks. Compared with the regular second-order Runge-Kutta method (RK2), our AETD2 method can use time steps one order of magnitude larger and improve computational efficiency more than ten times while excellently capturing accurate traces of membrane potentials of HH neurons. This high accuracy and efficiency can be robustly obtained and do not depend on the dynamical regimes, connectivity structure or the network size.Background Functional neurological disorders are characterized by neurological symptoms that have no identifiable pathology and little is known about their underlying pathophysiology. Objectives To analyze motor cortex excitability and intracortical inhibitory and excitatory circuits' imbalance in patients with flaccid functional weakness. selleck products Methods Twenty-one consecutive patients with acute onset of flaccid functional weakness were recruited. Single and paired-pulse transcranial magnetic stimulation (TMS) protocols were used to analyze resting motor thresholds (RMT) and intracortical inhibitory (short interval intracortical inhibition - SICI) and excitatory (intracortical facilitation - ICF) circuits' imbalance between the affected and non-affected motor cortices. Results We observed a significant increase in RMT and SICI in the affected motor cortex (p less then 0.001), but not for ICF, compared to the contralateral unaffected side. Conclusion This study extends current knowledge of functional weakness, arguing for a specific central nervous system abnormality which may be involved in the symptoms' pathophysiology.In the advent of intelligent robotic tools for physically assisting humans, user experience, and intuitiveness in particular have become important features for control designs. link2 However, existing works predominantly focus on performance-related measures for evaluating control systems as the subjective experience of a user by large cannot be directly observed. In this study, we therefore focus on agency-related interactions between control and embodiment in the context of physical human-machine interaction. By applying an intentional binding paradigm in a virtual, machine-assisted reaching task, we evaluate how the sense of agency of able-bodied humans is modulated by assistive force characteristics of a physically coupled device. In addition to measuring how assistive force profiles influence the sense of agency with intentional binding, we analyzed the sense of agency using a questionnaire. Remarkably, our participants reported to experience stronger agency when being appropriately assisted, although they contributed less to the control task. This is substantiated by the overall consistency of intentional binding results and the self-reported sense of agency. Our results confirm the fundamental feasibility of the sense of agency to objectively evaluate the quality of human-in-the-loop control for assistive technologies. While the underlying mechanisms causing the perceptual bias observed in the intentional binding paradigm are still to be understood, we believe that this study distinctly contributes to demonstrating how the sense of agency characterizes intuitiveness of assistance in physical human-machine interaction.Dysfunction and dysregulation at the genetic, neural, and behavioral levels point at the fine-tuning of broadly spread networks as critical for a wide array of behaviors and mental processes through the life span. This brain-based evidence, from basic to behavioral neuroscience levels, is leading to a new conceptualization of mental health and disease. Thus, the Research Domain Criteria considers phenotypic differences observed among disorders as explained by variations in the nature and degree of neural circuitry disruptions, under the modulation of several developmental, compensatory, environmental, and epigenetic factors. link3 In this context, we aimed to describe for the first time the in vivo behavioral impact of tweaking the PI3K/Akt signaling pathway known to play an essential role in the regulation of cellular processes, leading to diverse physiological responses. We explored the effects in young (YA, 3-4 months of age) and mature (MA, 11-14 months of age) male and female PDK1 K465E knock-in mice in a battory factor.The purpose of the present study is to investigate the influence of music tempo on inhibition control. An electroencephalogram (EEG) was recorded when participants performed a Go/No-go task while listening to slow (54 bpm), medium-paced (104 bpm), fast (154 bpm), or no music. The behavioral results showed that the accuracies for the No-go trials were lower in the fast than in the slow tempo music conditions, while the accuracies for the Go trials were also lower in the fast tempo than in no music conditions. The event-related potential (ERP) study results showed that larger N2 and P3 amplitudes were elicited by No-go than by Go conditions. Moreover, the difference N2 (N2d) amplitudes observed by No-go vs. Go condition were larger in fast music than in medium-paced, slow, and no music conditions, indicating more consumption of cognitive resources in the process of conflict monitoring under the fast music condition. However, no such differences were observed among medium-paced, slow, and no music conditions. In addition, the difference P3 (P3d) amplitudes, an index of response inhibition, were not significant among these four music conditions. The present study showed a detrimental influence of music tempo on inhibition control. More specifically, listening to fast music might impair an individual's ability to monitor conflict when performing the inhibitory control task.Temporomandibular joint disorder (TMD) is associated with pain in the joint (temporomandibular joint, TMJ) and muscles involved in mastication. TMD pain dissipates following menopause but returns in some women undergoing estrogen replacement therapy. Progesterone has both anti-inflammatory and antinociceptive properties, while estrogen's effects on nociception are variable and highly dependent on both natural hormone fluctuations and estrogen dosage during pharmacological treatments, with high doses increasing pain. Allopregnanolone, a progesterone metabolite and positive allosteric modulator of the GABAA receptor, also has antinociceptive properties. While progesterone and allopregnanolone are antinociceptive, their effect on estrogen-exacerbated TMD pain has not been determined. We hypothesized that removing the source of endogenous ovarian hormones would reduce inflammatory allodynia in the TMJ of rats and both progesterone and allopregnanolone would attenuate the estrogen-provoked return of allodynia. Basalso administered either daily or every other day. Allopregnanolone treatment, whether daily or every other day, also attenuated estrogen-exacerbated allodynia within 1 h of treatment, but only on the first treatment day. These data indicate that when gonadal hormone levels have diminished, treatment with a lower dose of progesterone may be effective at rapidly reducing the estrogen-evoked recurrence of inflammatory mechanical allodynia in the TMJ.In this review article, we highlight several disparate ideas that are linked to changes in brain state (i.e., sleep to arousal, Down to Up, synchronized to de-synchronized). In any discussion of the brain state, we propose that the cortical pyramidal neuron has a central position. EEG recordings, which typically assess brain state, predominantly reflect the activity of cortical pyramidal neurons. This means that the dominant rhythmic activity that characterizes a particular brain state ultimately has to manifest globally across the pyramidal neuron population. During state transitions, it is the long-range connectivity of these neurons that broadcast the resultant changes in activity to many subcortical targets. Structures like the thalamus, brainstem/hypothalamic neuromodulatory systems, and respiratory systems can also strongly influence brain state, and for many decades we have been uncovering bidirectional pathways that link these structures to state changes in the cerebral cortex. More recently, movement and active behaviors have emerged as powerful drivers of state changes. Each of these systems involve different circuits distributed across the brain. Yet, for a system-wide change in brain state, there must be a collaboration between these circuits that reflects and perhaps triggers the transition between brain states. As we expand our understanding of how brain state changes, our current challenge is to understand how these diverse sets of circuits and pathways interact to produce the changes observed in cortical pyramidal neurons.In the course of a day, brain states fluctuate, from conscious awake information-acquiring states to sleep states, during which previously acquired information is further processed and stored as memories. One hypothesis is that memories are consolidated and stored during "offline" states such as sleep, a process thought to involve transfer of information from the hippocampus to other cortical areas. Up and Down states (UDS), patterns of activity that occur under anesthesia and sleep states, are likely to play a role in this process, although the nature of this role remains unclear. Here we review what is currently known about these mechanisms in three anatomically distinct but interconnected cortical areas somatosensory cortex, entorhinal cortex, and the hippocampus. In doing so, we consider the role of this activity in the coordination of "replay" during sleep states, particularly during hippocampal sharp-wave ripples. We conclude that understanding the generation and propagation of UDS may provide key insights into the cortico-hippocampal dialogue linking archi- and neocortical areas during memory formation.Linking neural circuitry to behavior by mapping active neurons in vivo is a challenge. Both genetically encoded calcium indicators (GECIs) and intermediate early genes (IEGs) have been used to pinpoint active neurons during a stimulus or behavior but have drawbacks such as limiting the movement of the organism, requiring a priori knowledge of the active region or having poor temporal resolution. Calcium-modulated photoactivatable ratiometric integrator (CaMPARI) was engineered to overcome these spatial-temporal challenges. CaMPARI is a photoconvertible protein that only converts from green to red fluorescence in the presence of high calcium concentration and 405 nm light. This allows the experimenter to precisely mark active neurons within defined temporal windows. The photoconversion can then be quantified by taking the ratio of the red fluorescence to the green. CaMPARI promises the ability to trace active neurons during a specific stimulus; however, CaMPARI's uses in adult Drosophila have been limited to photoconversion during fly immobilization.
Homepage: https://www.selleckchem.com/products/Dasatinib.html
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