Neuroscience
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Closed-loop approaches, setups, and experimental designs have been applied within the field of neuroscience to enhance the understanding of basic neurophysiology principles (closed-loop neuroscience; CLNS) and to develop improved procedures for modulating brain circuits and networks for clinical purposes (closed-loop neuromodulation; CLNM). The contents of this review are thus arranged into the following sections. First, we describe basic research findings that have been made using CLNS. ⋯ Finally, we summarize methodological concerns and critics in clinical practice of neurofeedback and novel applications of closed-loop perspective and techniques to improve and optimize its experiments. Moreover, we outline the theoretical explanations and experimental ideas to test animal models of neurofeedback and discuss technical issues and challenges associated with implementing closed-loop systems. We hope this review is helpful for both basic neuroscientists and clinical/ translationally-oriented scientists interested in applying closed-loop methods to improve mental health and well-being.
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The highest disability rates and mortality among neurodegenerative diseases were caused by intracerebral hemorrhage (ICH). We previously proved that Benzene, 1,2,4-trimethoxy-5-(2-methyl-1-propen-1-yl) (BTY) has an inhibitory effect on sodium ion channel and an activation effect on GABAA receptor, which were related to the brain injury. Based on this, we aimed to investigate BTY's neuroprotection on intracerebral hemorrhage and its underlying mechanism. ⋯ The results showed that the BTY reduced brain edema and hematoma volume, improved neurological function and BBB permeability, and inhibited inflammatory factors and neuron apoptosis. The cell experiments proved that the BTY suppressed oxidative stress, cell apoptosis, intracellular calcium influx, and stabilized mitochondrial membrane potential by reducing glutamate's excitotoxicity. This study for the first time exhibited desirable neuroprotection of BTY, indicating it may be a promising neuroprotective agent for ICH therapy.
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It has been shown that a previously consolidated memory can incorporate either new external information or a novel internal emotional state following a labile state induced by retrieval. This updating process allows editing unwanted fear memory, leading to the reduction of the fear response. Memory can be modulated by the circadian cycle. ⋯ However, three retrieval sessions in the dark cycle were able to update fear memory, reducing freezing response in the test performed in the light cycle. This effect was blocked when the glucocorticoid synthesis inhibitor metyrapone was administered before retrieval. This approach opens new avenues to explore interventions that consider the circadian cycle in the treatment of fear memories based on non-pharmacological interventions.
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The inflammatory response of central nervous system (CNS) and microglial activation is important in the development of pain behaviors induced by sleep deprivation. We found that chronic sleep deprivation (CSD) aggravated pain behaviors in rats with chronic pain by upregulating expression of Toll-like receptor 4 (TLR4), NOD-like receptor pyrin domain containing 3 (NLRP3), and interleukin 1β (IL-1β), which promoted microglial activation in the brain. ⋯ Inhibitors of TLR4 and NLRP3 (TAK-242 and MCC950, respectively) reduced expression levels of inflammatory factor proteins and M1-related factor mRNA, decreased microglial activation, and relieved the hyperalgesia caused by CSD. These results suggest that CSD aggravated pain behavior in rats with chronic pain through the TLR4/NLRP3/IL-1β signaling pathway, which mediates microglial activation and promotes CNS inflammation and neuronal apoptosis.
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The mismatch negativity (MMN) component of the human event-related potential (ERP) is frequently interpreted as a sensory prediction-error signal. However, there is ambiguity concerning the neurophysiology underlying hypothetical prediction and prediction-error signalling components, and whether these can be dissociated from overlapping obligatory components of the ERP that are sensitive to physical properties of sounds. In the present study, a hierarchical recurrent neural network (RNN) was fitted to ERP data from 38 subjects. ⋯ Hidden units were categorised according to their temporal response fields, and statistically significant differences among stimulus conditions were observed for amplitudes of units peaking in the 0-75 ms (P50), 75-125 ms (N1), and 250-400 ms (N3) latency ranges, surprisingly not including the measurement window of MMN. The model demonstrated opposite polarity changes in MMN amplitude produced by falling (70 dB) and rising (90 dB) intensity deviant stimuli, consistent with loudness dependence of sensory ERP components. This modelling study suggests that loudness dependence is a principal driver of intensity MMN, and future studies ought to clarify the distinction between loudness dependence, adaptation and prediction-error signalling.