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Introduction Alterations in narrow‐band spectral power of electroencephalography (EEG) recordings are commonly reported in patients with schizophrenia (SZ). It is well established however that electrophysiological signals comprise a broadband scale‐free (or fractal) component generated by mechanisms different from those producing oscillatory neural activity. Despite this known feature, it has not yet been investigated if spectral abnormalities found in SZ could be attributed to scale‐free or oscillatory brain function. Methods In this study, we analyzed resting‐state EEG recordings of 14 SZ patients and 14 healthy controls. Scale‐free and oscillatory components of the power spectral density (PSD) were separated, and band‐limited power (BLP) of the original (mixed) PSD, as well as its fractal and oscillatory components, was estimated in five frequency bands. The scaling property of the fractal component was characterized by its spectral exponent in two distinct frequency ranges (1–13 and 13–30 Hz). Results Analysis of the mixed PSD revealed a decrease of BLP in the delta band in SZ over the central regions; however, this difference could be attributed almost exclusively to a shift of power toward higher frequencies in the fractal component. Broadband neural activity expressed a true bimodal nature in all except frontal regions. Furthermore, both low‐ and high‐range spectral exponents exhibited a characteristic topology over the cortex in both groups. Conclusion Our results imply strong functional significance of scale‐free neural activity in SZ and suggest that abnormalities in PSD may emerge from alterations of the fractal and not only the oscillatory components of neural activity. In this study, we separated the scale‐free (fractal) and oscillatory components of the power spectral density (PSD) of electroencephalography recordings acquired from healthy controls (HC) and patients with schizophrenia (SZ). We found increased delta band‐limited power in SZ when compared to HC in the raw PSD; however, this difference was only present in its fractal but not its oscillatory component. Our results imply strong functional significance of scale‐free neural activity in SZ and suggest that abnormalities in PSD may emerge from alterations of the fractal and not only the oscillatory components of neural activity.

Introduction As aging attracted attention globally, revealing changes in brain function across the lifespan was largely concerned. In this study, we aimed to reveal the changes of functional networks of the brain (via local functional connectivity, local FC) in lifespan and explore the mechanism underlying them. Materials and Methods A total of 523 healthy participants (258 males and 265 females) aged 18–88 years from part of the Cambridge Center for Ageing and Neuroscience (CamCAN) were involved in this study. Next, two data‐driven measures of local FC, local functional connectivity density (lFCD) and four‐dimensional spatial‐temporal consistency of local neural activity (FOCA), were calculated, and then, general linear models were used to assess the changes of them in lifespan. Results Local functional connectivity (lFCD and FOCA) within visual networks (VN), sensorimotor network (SMN), and default mode network (DMN) decreased across the lifespan, while within basal ganglia network (BGN), local connectivity was increased across the lifespan. And, the fluid intelligence decreased within BGN while increased within VN, SMN, and DMN. Conclusion These results might suggest that the decline of executive control and intrinsic cognitive ability in the aging population was related to the decline of functional connectivity in VN, SMN, and DMN. Meanwhile, BGN might play a regulatory role in the aging process to compensate for the dysfunction of other functional systems. Our findings may provide important neuroimaging evidence for exploring the brain functional mechanism in lifespan. We used local functional connectivity (FCD and FOCA) to explore changes across the lifespan and behavior scores (fluid intelligence and response time in response time tasks). Our findings may provide important neuroimaging evidence for exploring the brain functional connectivity mechanism across the lifespan.

Face and body perception is mediated by configural mechanisms, which allow the perception of these stimuli as a whole, rather than the sum of individual parts. Indirect measures of configural processing in visual cognition are the face and body inversion effects (FIE and BIE), which refer to the drop in performance when these stimuli are perceived upside-down. Albeit FIE and BIE have been well characterized at the behavioral level, much still needs to be understood in terms of the neurophysiological correlates of these effects. Thus, in the current study, the brain's electrical activity has been recorded by a 128 channel electroencephalogram (EEG) in 24 healthy participants while perceiving (upright and inverted) faces, bodies and houses. EEG data were analyzed in both the time domain (i.e., event-related potentials-ERPs) and the frequency domain [i.e., induced theta (5-7 Hz) and gamma (28-45 Hz) oscillations]. ERPs amplitude results showed increased N170 amplitude for inverted faces and bodies (compared to the same stimuli presented in canonical position) but not for houses. ERPs latency results showed delayed N170 components for inverted (vs. upright) faces, houses, but not bodies. Spectral analysis of induced oscillations indicated physiological FIE and BIE; that is decreased gamma-band synchronization over right occipito-temporal electrodes for inverted (vs. upright) faces, and increased bilateral frontoparietal theta-band synchronization for inverted (vs. upright) faces. Furthermore, increased left occipito-temporal and right frontal theta-band synchronization for upright (vs. inverted) bodies was found. Our findings, thus, demonstrate clear differences in the neurophysiological correlates of face and body perception. The neurophysiological FIE suggests disruption of feature binding processes (decrease in occipital gamma oscillations for inverted faces), together with enhanced feature-based attention (increase in frontoparietal theta oscillations for inverted faces). In contrast, the BIE may suggest that structural encoding for bodies is mediated by the first stages of configural processing (decrease in occipital theta oscillations for inverted bodies).

Motor neurons are the site of action for several neurological disorders and paralytic toxins, with cell bodies located in the ventral horn (VH) of the spinal cord along with interneurons and support cells. Microelectrode arrays (MEAs) have emerged as a high content assay platform for mechanistic studies and drug discovery. Here, we explored the spontaneous and evoked electrical activity of VH cultures derived from embryonic mouse spinal cord on multi-well plates of MEAs. Primary VH cultures from embryonic day 15-16 mice were characterized by expression of choline acetyltransferase (ChAT) by immunocytochemistry. Well resolved, all-or-nothing spontaneous spikes with profiles consistent with extracellular action potentials were observed after 3 days , persisting with consistent firing rates until at least day 19. The majority of the spontaneous activity consisted of tonic firing interspersed with coordinated bursting across the network. After 5 days , spike activity was readily evoked by voltage pulses where a minimum amplitude and duration required for excitation was 300 mV and 100 μs/phase, respectively. We characterized the sensitivity of spontaneous and evoked activity to a host of pharmacological agents including AP5, CNQX, strychnine, ω-agatoxin IVA, and botulinum neurotoxin serotype A (BoNT/A). These experiments revealed sensitivity of the cultured VH to both agonist and antagonist compounds in a manner consistent with mature tissue derived from slices. In the case of BoNT/A, we also demonstrated intoxication persistence over an 18-day period, followed by partial intoxication recovery induced by N- and P/Q-type calcium channel agonist GV-58. In total, our findings suggest that VH cultures on multi-well MEA plates may represent a moderate throughput, high content assay for performing mechanistic studies and for screening potential therapeutics pertaining to paralytic toxins and neurological disorders.

Stroke causes long-term disability, and rehabilitative training is commonly used to improve the consecutive functional recovery. Following brain damage, surviving neurons undergo morphological alterations to reconstruct the remaining neural network. In the motor system, such neural network remodeling is observed as a motor map reorganization. Because of its significant correlation with functional recovery, motor map reorganization has been regarded as a key phenomenon for functional recovery after stroke. Although the mechanism underlying motor map reorganization remains unclear, increasing evidence has shown a critical role for axonal remodeling in the corticospinal tract. In this study, we review previous studies investigating axonal remodeling in the corticospinal tract after stroke and discuss which mechanisms may underlie the stimulatory effect of rehabilitative training. Axonal remodeling in the corticospinal tract can be classified into three types based on the location and the original targets of corticospinal neurons, and it seems that all the surviving corticospinal neurons in both ipsilesional and contralesional hemisphere can participate in axonal remodeling and motor map reorganization. Through axonal remodeling, corticospinal neurons alter their output selectivity from a single to multiple areas to compensate for the lost function. The remodeling of the corticospinal axon is influenced by the extent of tissue destruction and promoted by various therapeutic interventions, including rehabilitative training. Although the precise molecular mechanism underlying rehabilitation-promoted axonal remodeling remains elusive, previous data suggest that rehabilitative training promotes axonal remodeling by upregulating growth-promoting and downregulating growth-inhibiting signals.

Exercise enhances hippocampal function, which is critical for learning, memory, and dementia prevention. However, the effects of exercise depend not only on intensity and frequency but also on the type of exercise, and not all exercise paradigms reliably activate hippocampal circuits. We compared treadmill exercise (TE) and rotarod exercise (RE) in mice to determine whether exercise type differentially influences neural activity and hippocampal plasticity across brain regions, using acute and chronic exercise paradigms. In acute exercise experiments, TE robustly increased neuronal activation in the dorsal hippocampus and entorhinal cortex. In contrast, RE activated other brain regions, including the ventral hippocampus and dorsal raphe nucleus, but did not increase activity in the dorsal hippocampus-entorhinal pathway. In chronic phase experiments, both TE and RE produced antidepressant effects, whereas only TE stimulated hippocampal neurogenesis. These results demonstrate that the effects of exercise on the brain are determined by interactions between exercise type and brain region. The findings highlight region-specific and exercise type-dependent characteristics of exercise-induced brain plasticity, underscoring the importance of considering exercise type when aiming to promote hippocampal health and prevent dementia.

Cortical networks that have been found to operate close to a critical point exhibit joint activations of large numbers of neurons. However, in motor cortex of the awake macaque monkey, we observe very different dynamics: massively parallel recordings of 155 single-neuron spiking activities show weak fluctuations on the population level. This a priori suggests that motor cortex operates in a noncritical regime, which in models, has been found to be suboptimal for computational performance. However, here, we show the opposite: The large dispersion of correlations across neurons is the signature of a second critical regime. This regime exhibits a rich dynamical repertoire hidden from macroscopic brain signals but essential for high performance in such concepts as reservoir computing. An analytical link between the eigenvalue spectrum of the dynamics, the heterogeneity of connectivity, and the dispersion of correlations allows us to assess the closeness to the critical point.

Intercellular signaling molecules such as cytokines and their receptors enable immune cells to communicate with one another and their surrounding microenvironments. Emerging evidence suggests that the same signaling pathways that regulate inflammatory responses to injury and disease outside of the brain also play powerful roles in brain development, plasticity, and function. These observations raise the question of how the same signaling molecules can play such distinct roles in peripheral tissues compared to the central nervous system, a system previously thought to be largely protected from inflammatory signaling. Here, we review evidence that the specialized roles of immune signaling molecules such as cytokines in the brain are to a large extent shaped by neural activity, a key feature of the brain that reflects active communication between neurons at synapses. We discuss the known mechanisms through which microglia, the resident immune cells of the brain, respond to increases and decreases in activity by engaging classical inflammatory signaling cascades to assemble, remodel, and eliminate synapses across the lifespan. We integrate evidence from (1) in vivo imaging studies of microglia-neuron interactions, (2) developmental studies across multiple neural circuits, and (3) molecular studies of activity-dependent gene expression in microglia and neurons to highlight the specific roles of activity in defining immune pathway function in the brain. Given that the repurposing of signaling pathways across different tissues may be an important evolutionary strategy to overcome the limited size of the genome, understanding how cytokine function is established and maintained in the brain could lead to key insights into neurological health and disease.

Neural interfaces, emerging at the intersection of neurotechnology and urban planning, promise to transform how we interact with our surroundings and communicate. By recording and decoding neural signals, these interfaces facilitate direct connections between the brain and external devices, enabling seamless information exchange and shared experiences. Nevertheless, their development is challenged by complexities in materials science, electrochemistry, and algorithmic design. Electrophysiological crosstalk and the mismatch between electrode rigidity and tissue flexibility further complicate signal fidelity and biocompatibility. Recent closed‐loop brain‐computer interfaces, while promising for mood regulation and cognitive enhancement, are limited by decoding accuracy and the adaptability of user interfaces. This perspective outlines these challenges and discusses the progress in neural interfaces, contrasting non‐invasive and invasive approaches, and explores the dynamics between stimulation and direct interfacing. Emphasis is placed on applications beyond healthcare, highlighting the need for implantable interfaces with high‐resolution recording and stimulation capabilities. This perspective explores diverse neural interfaces in the brain, offering transformative possibilities for engaging with our environment and enhancing communication. Emphasis is placed on the role of both non‐invasive and invasive neural interfaces in transforming practical applications beyond the realm of healthcare, emphasizing the promising implications for remote control, mind connectivity, and integrated urban design.

Thirst and hunger are fundamental survival drives that modulate various aspects of animal behavior through specific neural circuits. Previous studies have demonstrated that dopaminergic neurons (DANs) innervating the mushroom body (MB) in the Drosophila brain play essential roles in innate and learned thirst- and hunger-dependent behaviors, with most experiments focusing on acute water or food deprivation. However, it is unclear whether acute water or food deprivation alters dopamine production and neural activity in MB-innervating DANs. We genetically expressed green fluorescent protein (GFP) in MB-innervating DANs using broadly and specifically labeled GAL4 lines under satiety, thirst, and hunger states. The brains were immunostained with anti-tyrosine hydroxylase (TH) to assess dopamine biosynthesis. Additionally, the transcriptional reporter of intracellular Ca (TRIC) was expressed in these DANs using the same GAL4 lines to monitor neural activity under different internal states. Normalized anti-TH and TRIC signals in specific MB compartments were compared between the satiety and thirst groups and between the satiety and hunger groups using unpaired two-tailed t-tests. Neither TH levels nor neural activity in the 13 subtypes of MB-innervating DANs exhibited significant differences during the satiety, thirst, and hunger conditions. This study suggests that 16-hour water deprivation or 24-hour food deprivation does not significantly alter dopamine production and neural activity in MB-innervating DANs. These findings offer insights into the independence of baseline dopaminergic activity from internal states in thirst- or hunger-related behaviors.