Neuronal Activity In Brain Research Articles

Impaired cecal motility and secretion alongside expansion of gut-associated lymphoid tissue in the Nlgn3R451C mouse model of autism

Individuals with Autism Spectrum Disorder (ASD; autism) commonly present with gastrointestinal (GI) illness in addition to core diagnostic behavioural traits. The appendix, or cecum in mice, is important for GI homeostasis via its function as a key site for fermentation and a microbial reservoir. Even so, the role of the appendix and cecum in autism-associated GI symptoms remains uninvestigated. Here, we studied mice with an autism-associated missense mutation in the post-synaptic protein neuroligin-3 (Nlgn3R451C), which impacts brain and enteric neuronal activity. We assessed for changes in cecal motility using a tri-cannulation video-imaging approach in ex vivo preparations from wild-type and Nlgn3R451C mice. We investigated cecal permeability and neurally-evoked secretion in wild-type and Nlgn3R451C tissues using an Ussing chamber set-up. The number of cecal patches in fresh tissue samples were assessed and key immune populations including gut macrophages and dendritic cells were visualised using immunofluorescence. Nlgn3R451C mice displayed accelerated cecal motor complexes and reduced cecal weight in comparison to wildtype littermates. Nlgn3R451C mice also demonstrated reduced neurally-evoked cecal secretion in response to the nicotinic acetylcholine receptor agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP), but permeability was unchanged. We observed an increase in the number of cecal patches in Nlgn3R451C mice, however the cellular morphologies of key immune populations studied were not significantly altered. We show that the R451C nervous system mutation leads to cecal dysmotility, impaired secretion, and neuro-immune alterations. Together, these results suggest that the R451C mutation disrupts the gut-brain axis with GI dysfunction in autism.

Microscopic-scale magnetic recording of brain neuronal electrical activity using a diamond quantum sensor

Quantum sensors using solid state qubits have demonstrated outstanding sensitivity, beyond that possible using classical devices. In particular, those based on colour centres in diamond have demonstrated high sensitivity to magnetic field through exploiting the field-dependent emission of fluorescence under coherent control using microwaves. Given the highly biocompatible nature of diamond, sensing from biological samples is a key interdisciplinary application. In particular, the microscopic-scale study of living systems can be possible through recording of temperature and biomagnetic field. In this work, we use such a quantum sensor to demonstrate such microscopic-scale recording of electrical activity from neurons in fragile living brain tissue. By recording weak magnetic field induced by ionic currents in mouse corpus callosum axons, we accurately recover signals from neuronal action potential propagation while demonstrating in situ pharmacology. Our sensor allows recording of the electrical activity in neural circuits, disruption of which can shed light on the mechanisms of disease emergence. Unlike existing techniques for recording activity, which can require potentially damaging direct interaction, our sensing is entirely passive and remote from the sample. Our results open a promising new avenue for the microscopic recording of neuronal signals, offering the eventual prospect of microscopic imaging of electrical activity in the living mammalian brain.

Understanding the Brain-based Determination of Death When Organ Recovery Is Performed With DCDD In Situ Normothermic Regional Perfusion.

Understanding the Brain-based Determination of Death When Organ Recovery Is Performed With DCDD In Situ Normothermic Regional Perfusion.

Novel Pulsed-Ultrahigh-Frequency Spinal Cord Stimulation Inhibits Mechanical Hypersensitivity and Brain Neuronal Activity in Rats after Nerve Injury.

Spinal cord stimulation (SCS) is an important pain treatment modality. We hypothesized that a novel pulsed-ultrahigh-frequency SCS (pUHF-SCS) could safely and effectively inhibit spared nerve injury-induced neuropathic pain in rats. Epidural pUHF-SCS (± 3V, 2Hz pulses comprising 500 kHz biphasic sinewaves) was implanted at the thoracic vertebrae (T9-T11). Local field brain potentials following hind paw stimulation were recorded. Analgesia was evaluated by von-Frey-evoked allodynia and acetone-induced cold allodynia. The mechanical withdrawal threshold of the injured paw was 0.91 ± 0.28 g lower than that of the sham surgery (24.9 ± 1.2 g). Applying 5-, 10-, or 20-minute pUHF-SCS five times every two days significantly increased the paw withdrawal threshold to 13.3 ± 6.5, 18.5 ± 3.6, and 21.0 ± 2.8 g at 5 hours post-SCS, respectively (p = 0.0002, < 0.0001, and < 0.0001; n = 6/group), and to 6.1 ± 2.5, 8.2 ± 2.7, and 14.3 ± 5.9 g on the second day, respectively (p = 0.123, 0.013, and < 0.0001). Acetone-induced paw response numbers decreased from pre-SCS (41 ± 12) to 24 ± 12 and 28 ± 10 (p = 0.006 and 0.027; n = 9) at 1 and 5 hours post-three rounds of 20-minute pUHF-SCS, respectively. The areas under the curve from the C component of the evoked potentials at the left primary somatosensory and anterior cingulate cortices were significantly decreased from pre-SCS (101.3 ± 58.3 and 86.9 ± 25.5, respectively) to 39.7 ± 40.3 and 36.3 ± 20.7 (p = 0.021, and 0.003; n = 5) at 60 minutes post-SCS, respectively. The intensity thresholds for pUHF-SCS to induce brain and sciatic nerve activations were much higher than the therapeutic intensities and thresholds of conventional low-frequency SCS. pUHF-SCS inhibited neuropathic pain-related behavior and paw stimulation evoked brain activation through mechanisms distinct from low-frequency SCS.

Концепция человека и его духовности в современных нейронаучных исследованиях: философский анализ

The article is devoted to a critical review of a qualitatively new project of human understanding, which has been developed in modern scientific interdisciplinary research. The latter refers to neuroscience research that affects not only neurophysiology, but also claims to revolutionize the philosophical understanding of human nature and spirituality. This revolution concerns, first of all, the interpretation of spirituality as a special subjective reality, as well as the solution of the so-called "hard mind problem" ("complex problem of consciousness"). The author turns to the analysis of the concept of spirituality, which is interpreted in the context of neuroscientific research on subjective reality. Spirituality in these studies is identified with subjective reality. In the neurosciences, spirituality as a sphere of human existence, aimed at transcendental values, is replaced by subjective reality, which ultimately comes down to the activity of brain neurons. The author gives a critical assessment of this interpretation of spirituality. A special place in understanding the subjective reality of neuroscience is assigned to the problem of consciousness. The author analyzes the solution of the "complex problem of consciousness" from the standpoint of modern neuroscience. In this regard, special attention is paid to the concept of neuropsychoanalysis by Mark Solms. The author considers the concept of Marx Solms as one of the many reductionist projects that exist in modern science, reducing human nature to biological and neurophysiological processes occurring in the brain. The author points out that such reductionism leads not only to a rethinking of human nature, but also to a new vector in the development of modern philosophical anthropology – as a secondary doctrine of man that complements neuroscience.

Revealing the coupling directionality and synchronization between time series from physiological data by analysis of joint recurrences

We applied methods for determining the recurrence based phase synchronization index and the coupling directionality based on conditional probabilities of recurrence to analyze the direction of coupling and synchronization of time series obtained from experimental data. The activity of brain neurons, fluctuations in arterial blood pressure, and the respiratory rhythm of anesthetized rats were used as experimental data. For the first time, variants of changing the direction of the coupling between the analyzed time series before and during pain exposure were revealed. The relationship of pain exposure with the adjustment of the frequency of the variability of neuron activity of the brain to the frequency of the variability of arterial blood pressure or with the adjustment of the frequency of the variability of blood pressure to the respiratory rhythm with the subsequent occurrence of phase synchronization has been established.

Advanced prodrug approaches for neurodegenerative diseases

The prodrug technique is still one of the most effective ways to increase hydrophilic substances' medicinal, pharmacodynamic and pharmacokinetic properties. Prodrugs produced in current history have shown good pharmacokinetic characteristics, allowing for a more consistent release and fewer changes in plasma levels. Developing new prodrugs having a desirable ADME (Absorption Distribution Metabolism and Elimination) properties and that still can cross the Blood brain barrier (BBB) and pharmacologically active an appealing task for medicinal chemists. The loss of brain neuron activity characterizes neurodegenerative illnesses, resulting in progressive Gradual cognitive impairment (GCI). Some of the common neurodegenerative diseases are PD (Parkinson's disease), AD (Alzheimer's disease), MS (Multiple sclerosis), ALS (amyotrophic lateral sclerosis) &amp; HD (Huntington's disease) are examples of neurodegenerative illnesses with a variety of etiologies and morphological and pathophysiological aspects. The current review is concerned with current advances in prodrug approaches for the treatment and prevention of the most prevalent neurological illnesses, as well as their absorption, selective CNS targeting and chemical and enzymatic stability.

Study on the Role of an Erythrocyte Membrane-Coated Nanotheranostic System in Targeted Immune Regulation of Alzheimer's Disease.

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases in the elderly population. Despite significant advances in studies of the pathobiology on AD, there is still no effective treatment. Here, an erythrocyte membrane-camouflaged nanodrug delivery system (TR-ZRA) modified with transferrin receptor aptamers that can be targeted across the blood-brain barrier to ameliorate AD immune environment is established. Based on metal-organic framework (Zn-CA), TR-ZRA is loaded with CD22shRNA plasmid to silence the abnormally high expression molecule CD22 in aging microglia. Most importantly, TR-ZRA can enhance the ability of microglia to phagocytose Aβ and alleviate complement activation, which can promote neuronal activity and decrease inflammation level in the AD brain. Moreover, TR-ZRA is also loaded with Aβ aptamers, which allow rapid and low-cost monitoring of Aβ plaques in vitro. After treatment with TR-ZRA, learning, and memory abilities are enhanced in AD mice. In conclusion, the biomimetic delivery nanosystem TR-ZRA in this study provides a promising strategy and novel immune targets for AD therapy.

The Abuse of Neurodegeneration Disease and How CRISPR-Cas9 Could Help with The Disease

Neurodegenerative disease has been discovered for more than a hundred years. This disease gradually damages the brain neuron activity and leads to death. There is no way to entirely heal the disease currently but scientists are still looking for some methods to slow it down and heal from it. More hope appears after the third generation of gene editing technology-CRISPR-Cas9- is discovered. This is a natural gene editing technology by CRISPR gene and Cas9 protein in the body with more precision and less cost than the previous two generations. CRISPR-Cas9 technology is based on the natural body system that detects and prevents virus RNA, and targets a precise sequence of genes to accomplish gene editing. Researchers believe that the damage of neurons by the disease could be slowed down or even stopped by knocking out the neurodegeneration related gene and knocking in desired healthy genes. Huntington disease, one of the most popular diseases in neurodegenerative disease, has been discovered relatively more. This research review focuses on the history of CRISPR-Cas9 gene editing technology and how it helps with neurodegenerative disease, especially with Huntington Disease.

As without, so within: how the brain's temporo-spatial alignment to the environment shapes consciousness.

Consciousness is constituted by a structure that includes contents as foreground and the environment as background. This structural relation between the experiential foreground and background presupposes a relationship between the brain and the environment, often neglected in theories of consciousness. The temporo-spatial theory of consciousness addresses the brain-environment relation by a concept labelled 'temporo-spatial alignment'. Briefly, temporo-spatial alignment refers to the brain's neuronal activity's interaction with and adaption to interoceptive bodily and exteroceptive environmental stimuli, including their symmetry as key for consciousness. Combining theory and empirical data, this article attempts to demonstrate the yet unclear neuro-phenomenal mechanisms of temporo-spatial alignment. First, we suggest three neuronal layers of the brain's temporo-spatial alignment to the environment. These neuronal layers span across a continuum from longer to shorter timescales. (i) The background layer comprises longer and more powerful timescales mediating topographic-dynamic similarities between different subjects' brains. (ii) The intermediate layer includes a mixture of medium-scaled timescales allowing for stochastic matching between environmental inputs and neuronal activity through the brain's intrinsic neuronal timescales and temporal receptive windows. (iii) The foreground layer comprises shorter and less powerful timescales for neuronal entrainment of stimuli temporal onset through neuronal phase shifting and resetting. Second, we elaborate on how the three neuronal layers of temporo-spatial alignment correspond to their respective phenomenal layers of consciousness. (i) The inter-subjectively shared contextual background of consciousness. (ii) An intermediate layer that mediates the relationship between different contents of consciousness. (iii) A foreground layer that includes specific fast-changing contents of consciousness. Overall, temporo-spatial alignment may provide a mechanism whose different neuronal layers modulate corresponding phenomenal layers of consciousness. Temporo-spatial alignment can provide a bridging principle for linking physical-energetic (free energy), dynamic (symmetry), neuronal (three layers of distinct time-space scales) and phenomenal (form featured by background-intermediate-foreground) mechanisms of consciousness.

Transcriptomic cell type structures in vivo neuronal activity across multiple timescales

Cell type is hypothesized to be a key determinant of a neuron's role within a circuit. Here, we examine whether a neuron's transcriptomic type influences the timing of its activity. We develop a deep-learning architecture that learns features of interevent intervals across timescales (ms to >30min). We show that transcriptomic cell-class information is embedded in the timing of single neuron activity in the intact brain of behaving animals (calcium imaging and extracellular electrophysiology) as well as in a bio-realistic model of the visual cortex. Further, a subset of excitatory cell types are distinguishable but can be classified with higher accuracy when considering cortical layer and projection class. Finally, we show that computational fingerprints of cell types may be universalizable across structured stimuli and naturalistic movies. Our results indicate that transcriptomic class and type may be imprinted in the timing of single neuron activity across diverse stimuli.

Behavioral phenotype, intestinal microbiome, and brain neuronal activity of male serotonin transporter knockout mice

The serotonin transporter (5-HTT) plays a critical role in the regulation of serotonin neurotransmission. Mice genetically deficient in 5-HTT expression have been used to study the physiological functions of 5-HTT in the brain and have been proposed as a potential animal model for neuropsychiatric and neurodevelopmental disorders. Recent studies have provided evidence for a link between the gut-brain axis and mood disorders. However, the effects of 5-HTT deficiency on gut microbiota, brain function, and behavior remain to be fully characterized. Here we investigated the effects of 5-HTT deficiency on different types of behavior, the gut microbiome, and brain c-Fos expression as a marker of neuronal activation in response to the forced swim test for assessing depression-related behavior in male 5-HTT knockout mice. Behavioral analysis using a battery of 16 different tests showed that 5-HTT−/− mice exhibited markedly reduced locomotor activity, decreased pain sensitivity, reduced motor function, increased anxiety-like and depression-related behavior, altered social behavior in novel and familiar environments, normal working memory, enhanced spatial reference memory, and impaired fear memory compared to 5-HTT+/+ mice. 5-HTT+/− mice showed slightly reduced locomotor activity and impaired social behavior compared to 5-HTT+/+ mice. Analysis of 16S rRNA gene amplicons showed that 5-HTT−/− mice had altered gut microbiota abundances, such as a decrease in Allobaculum, Bifidobacterium, Clostridium sensu stricto, and Turicibacter, compared to 5-HTT+/+ mice. This study also showed that after exposure to the forced swim test, the number of c-Fos-positive cells was higher in the paraventricular thalamus and lateral hypothalamus and was lower in the prefrontal cortical regions, nucleus accumbens shell, dorsolateral septal nucleus, hippocampal regions, and ventromedial hypothalamus in 5-HTT−/− mice than in 5-HTT+/+ mice. These phenotypes of 5-HTT−/− mice partially recapitulate clinical observations in humans with major depressive disorder. The present findings indicate that 5-HTT-deficient mice serve as a good and valid animal model to study anxiety and depression with altered gut microbial composition and abnormal neuronal activity in the brain, highlighting the importance of 5-HTT in brain function and the mechanisms underlying the regulation of anxiety and depression.

Insights into the Involvement and Therapeutic Target Potential of the Dopamine System in the PosttraumaticStressDisorder.

Posttraumatic stress disorder (PTSD) is a neuropsychiatric disease closely related to life-threatening events and psychological stress. Re-experiencing, hyperarousal, avoidance, and numbness are the hallmark symptoms of PTSD, but their underlying neurological processes have not been clearly elucidated. Therefore, the identification and development of drugs for PTSD that targets brain neuronal activities have stalled. Considering that the persistent fear memory induced by traumatic stimulation causes high alertness, high arousal, and cognitive impairment of PTSD symptoms. While the midbrain dopamine system can affect physiological processes such as aversive fear memory learning, consolidation, persistence, and extinction, by altering the functions of the dopaminergic neurons, our viewpoint is that the dopamine system plays a considerable role in the PTSD occurrence and acts as a potential therapeutic target of the disorder. This paper reviews recent findings on the structural and functional connections between ventral tegmental area neurons and the core synaptic circuits involved in PTSD, gene polymorphisms related to the dopamine system that confer susceptibility to clinical PTSD. Moreover, the progress of research on medications that target the dopamine system as PTSD therapies is also discussed. Our goal is to offer some hints for early detection and assist in identifying novel, efficient approaches for treating PTSD.

Effects of neuromodulation-inspired mechanisms on the performance of deep neural networks in a spatial learning task

In recent years, the biological underpinnings of adaptive learning have been modeled, leading to faster model convergence and various behavioral benefits in tasks including spatial navigation and cue-reward association. Furthermore, studies have investigated how the neuromodulatory system, a major driver of synaptic plasticity and state-dependent changes in the brain neuronal activities, plays a role in training deep neural networks (DNNs). In this study, we extended previous studies on neuromodulation-inspired DNNs and explored the effects of neuromodulatory components on learning and single unit activities in a spatial learning task. Under the multiscale neuromodulatory framework, plastic components, dropout probability modulation, and learning rate decay were added to the single unit, layer, and whole network levels of DNN models, respectively. We observed behavioral benefits including faster learning and smaller error of ambulation. We then concluded that neuromodulatory components can affect learning trajectories, outcomes, and single unit activities, in a component- and hyperparameter-dependent manner.

ITRAQ and PRM-Based Comparative Proteomic Profiling of the Hippocampus in Rat Models of Epilepsy.

Epilepsy is a disease caused by paroxysmal abnormal supersynchronous electrical activity of brain neurons, and it is also one of the most common illnesses in neurology. Among the causes, hippocampal sclerosis may be one of the main causes of temporal lobe epilepsy. However, the pathogenesis of hippocampal sclerosis in epilepsy remains unclear. We established an epilepsy model by intraperitoneal injection of pentetrazol (PTZ) into Sprague-Dawley rats, and applied isobaric tags for relative and absolute quantitation (iTRAQ) technology to identify differentially expressed proteins (DEPs) in the hippocampus. We quantified a total of 3782 proteins. DEPs were defined as proteins with a fold change >1.2 (or <0.83) and a Q value (p-adjusted) <0.05. Comparing the epilepsy group and the control group, we identified 170 DEPs, comprising 109 upregulated and 61 downregulated proteins. According to bioinformatics analysis, the DEPs were primarily involved in long-term potentiation, the calcium signalling pathway, aldosterone synthesis and secretion, carbon metabolism, and dopaminergic synapses. Four of these proteins were validated using parallel reaction monitoring (PRM), including Glud1, Atp1a2, Prkcg and Arpc3. Our research results may provide further insight into the molecular pathology of hippocampal injury in epilepsy.

Integrated information theory and its application for analysis of brain neuron activity

Purpose of this review is to consider the possibility to apply the integrated information theory to investigate the brain neural activity. Earlier was shown that the integrated information amount Φ quantifies a degree of a dynamic complexity of a system and able to predict a level of its success defined by classic observable benchmarks. For this reason, a question arises about the application of the integrated information theory to analyse changes in brain spiking activity due the acquisition of new experience. Conclusion. The bases of the integrated information theory and its possible application in neurobiology to investigate the process of new experience acquisition were reviewed. It was shown that the amount of integrated information Φ is a metric which is able to quantify the dynamic complexity of brain neural networks increasing when the new experience is acquired. Methods, enaabling the practical calculation of Φ for spiking data, were proposed.

Neurovascular coupling changes in patients with magnetic resonance imaging negative focal epilepsy

Brain neuron activity is closely related to cerebral blood flow (CBF) changes. Alterations in the regional homogeneity (ReHo) and CBF occur in patients with magnetic resonance imaging negative focal epilepsy (FEP-MRI−). However, the coupling alterations of ReHo and CBF in FEP-MRI− remain unclear. The study aims to explore neurovascular coupling alterations and their clinical implication in FEP-MRI−.We collected resting-state magnetic resonance imaging (MRI) data from 31 healthy controls (HCs) and 48 patients with FEP-MRI−,including three-dimensional (3D) T1-weighted imaging, 3D arterial spin labeling (ASL) imaging,and resting-state functional MRI (rs-fMRI). The CBF and ReHo values were calculated from the ASL and rs-fMRI data, respectively. The CBF/ReHo ratio per voxel and whole-brain CBF-ReHo coupling were compared between the two groups. Correlation analysis involved the CBF/ReHo ratio and clinical indicators in FEP-MRI−.Patients with FEP-MRI− showed significantly increased cross-subject CBF-ReHo and global cross-voxel CBF-ReHo coupling. The CBF/ReHo ratio was higher in the bilateral orbitofrontal gyrus, right parietal lobe, and right middle frontal gyrus of patients with FEP-MRI−. Nevertheless, this ratio was lower in the bilateral supplementary motor areas, the left middle and posterior cingulate gyrus, and the right central sulcus cover. The CBF/ReHo ratio was markedly correlated with cognitive function, memory, intelligence, and epilepsy duration in the above abnormal brain regions.CBF/ReHo ratio may be useful as an indicator of neuropathological mechanisms. These results support the hypothesis that CBF/ReHo ratio relates to the neuropathological mechanisms of FEP-MRI−. Furthermore, it offers new perspectives for studying the mechanisms of MRI-negative epilepsy.

Neuroscience of consciousness: cognition, physics and philosophy of decoding the human brain

The biophysical roots of consciousness have been the subject of an ongoing debate for centuries. In order to understand the data, create novel experimental methodologies, and increase our ability to investigate this phenomenon of interest, the proposed theories must lead to empirical, repeatable, and testifiable studies. Contemporary theories of consciousness often do not relate to one another, and none of them has been distinguished as complete or proven empirically so far. The aim of this study is an investigation into some of the possible approaches that could merge neuronal brain activity with the laws of physics and some philosophical principles that may be associated with the emergence of consciousness in the first place. As a result, the relationship between consciousness and attention, working memory, access consciousness and phenomenal consciousness is evaluated. The contrast between conscious and unconscious perception, perceived visual inputs and subliminal ones is investigated to facilitate a discussion about the neural correlates of self-awareness. Consciousness as a global broadcast of information to integrated brain modules is being considered, as well as viewing a brain as a parallel information processor linked to attention inputs. Relationship between consciousness and attention is explored, as well as attention without consciousness and vice versa. Implications and shortcomings of the proposed approaches based on brain science, philosophy and quantum physics are also covered to shed some more light on this ever present experience of being conscious that everyone seems to self-witness but no one manages to adequately explain.

Physical and social enrichment influences the adaptability-related behaviors of black rockfish Sebastes schlegelii: An effect mediated by social behaviors, HPI axis and neurogenesis

Environmental enrichment is a promising method to increase fish ecological fitness in hatchery release and to improve fish welfare in the aquaculture industry. However, little is known about the effects of physical and social enrichment on fish behavioral development and the relevant regulatory mechanisms. To address this knowledge gap, a typical aquaculture fish, black rockfish Sebastes schlegelii, was exposed to contrasting environments (i.e., physically enriched environment vs. barren environment, and socially low-density environment vs. high-density environment) for six weeks. Subsequently, the adaptability-related behaviors and social interactions during the captive period were determined, and stress-related physiological parameters and neurogenesis-related gene markers were measured. In general, the fish from an enriched environment expressed significantly higher sheltering propensity and anti-predator ability while less risk-taking frequency than the fish from a barren environment. And meanwhile, the fish from a low-density environment presented significantly less risk-taking behavior and more anti-predator responses than high-density fish. A structurally barren environment significantly increased fish aggressive frequency and locomotor activity compared with an enriched environment, whereas the social environment did not affect fish social interactions. For physiological status, the hypothalamus-pituitary-interrenal (HPI) axis and corticosteroid receptor system activities of barren fish were significantly higher than those of enriched fish, and meanwhile, the high-density fish also presented significantly higher physiological stress than low-density fish. For neurogenesis processes, an enriched environment did not affect fish brain cell proliferation but increased telencephalon neuronal differentiation ratio and immature neuron number. In contrast, a low-density environment significantly stimulated cell proliferating activity in telencephalon but did not affect brain neuronal differentiation activity. These novel results verified the conspicuous effects of physical and social environments on the adaptability-related behaviors in aquaculture fish, and finally, we proposed a novel regulatory pathway for fish behavioral plasticity, i.e., environmental stimuli - social interactions - HPI axis - corticosteroid receptor system - neurogenesis - adaptability-related behaviors. These results may lay the foundations for restoring fishery resources and for improving fish welfare, add novel knowledge to fish biology and environmental enrichment framework, and help deeply understand the mechanisms of environmental effects on marine animal behaviors.

Structural and functional alterations in cerebral small vessel disease: an ALE-based meta-analysis.

• Default mode network and salience network are reliable networks affected in sporadic CSVD in resting-state.• Altered corticostriatal circuitry is associated with cognitive decline.• Decreased gray matter volume in the insular cortex is stable "remote effects" of sporadic CSVD.• The parahippocampal gyrus may be a reliable affected brain region in CADASIL.