Level Of Spontaneous Activity Research Articles

Bugs on Drugs: Paracetamol Exposure Reveals Genotype-Specific Generational Effects on Life History Traits in Drosophila melanogaster.

Few investigations have been made to determine whether pharmaceutical drugs cause any generational effects. These effects can be divided into intergenerational and transgenerational effects. In insects, the F1 offspring of exposed individuals are considered to show intergenerational effects (as they have been exposed as germ cells or early embryos), while the F2 generation is fully non-exposed and considered to show transgenerational effects. Here, the common over-the-counter (OTC) drug, paracetamol, is investigated for genotype-specific responses and effects across generations on three life-history traits: fecundity, longevity, and spontaneous locomotor activity levels in the model species Drosophila melanogaster. Seven isofemale D. melanogaster lines were exposed to a high and intermediate dose of paracetamol determined by a dose-response curve. NMR investigations verified the long-term presence of paracetamol in the food substrate. Phenotypic effects of paracetamol ingestion were investigated on flies exposed to the drug and in their offspring and grand-offspring. The dose-response curve indicated genotype-specific responses to paracetamol. In the following experiment, all traits investigated displayed significant effects of paracetamol ingestion for at least one of the seven isofemale lines, and we detected strong genotype-specific responses to paracetamol. Fecundity tended to increase in individuals directly exposed to the drug whereas fecundity in the F2 generation was reduced (transgenerational). Longevity generally decreased in directly exposed individuals but tended to increase in F1 offspring (intergenerational). Paracetamol effects on spontaneous locomotor activity were primarily detected as transgenerational effects and were rarely seen in directly exposed individuals. However, across lines, no clear overall trend could be determined for any trait. The generational effects and marked genotype-specific response to paracetamol warrants further investigation of both genotype-specific responses and generational effects in general.

Spontaneous cortical activity is altered in persons with HIV and related to domain-specific cognitive function.

Whilst the average lifespan of persons with HIV now approximates that of the general population, these individuals are at a much higher risk of developing cognitive impairment with ∼35-70% experiencing at least subtle cognitive deficits. Previous works suggest that HIV impacts both low-level primary sensory regions and higher-level association cortices. Notably, multiple neuroHIV studies have reported elevated levels of spontaneous cortical activity during the pre-stimulus baseline period of task-based experiments, but only a few have examined such activity during resting-state conditions. In the current study, we examined such spontaneous cortical activity using magnetoencephalography in 79 persons with HIV and 83 demographically matched seronegative controls and related this neural activity to performance on neuropsychological assessments of cognitive function. Consistent with previous works, persons with HIV exhibited stronger spontaneous gamma activity, particularly in inferior parietal, prefrontal and superior temporal cortices. In addition, serostatus moderated the relationship between spontaneous beta activity and attention, motor and processing speed scores, with controls but not persons with HIV showing stronger beta activity with better performance. The current results suggest that HIV predominantly impacts spontaneous activity in association cortices, consistent with alterations in higher-order brain function, and may be attributable to deficient GABAergic signalling, given its known role in the generation of gamma and beta oscillations. Overall, these effects align with previous studies showing aberrant spontaneous activity in persons with HIV and provide a critical new linkage to domain-specific cognitive dysfunction.

Mice with deficiency in Pcdh15, a gene associated with bipolar disorders, exhibit significantly elevated diurnal amplitudes of locomotion and body temperature

Genetic factors significantly affect the pathogenesis of psychiatric disorders. However, the specific pathogenic mechanisms underlying these effects are not fully understood. Recent extensive genomic studies have implicated the protocadherin-related 15 (PCDH15) gene in the onset of psychiatric disorders, such as bipolar disorder (BD). To further investigate the pathogenesis of these psychiatric disorders, we developed a mouse model lacking Pcdh15. Notably, although PCDH15 is primarily identified as the causative gene of Usher syndrome, which presents with visual and auditory impairments, our mice with Pcdh15 homozygous deletion (Pcdh15-null) did not exhibit observable structural abnormalities in either the retina or the inner ear. The Pcdh15-null mice showed very high levels of spontaneous motor activity which was too disturbed to perform standard behavioral testing. However, the Pcdh15 heterozygous deletion mice (Pcdh15-het) exhibited enhanced spontaneous locomotor activity, reduced prepulse inhibition, and diminished cliff avoidance behavior. These observations agreed with the symptoms observed in patients with various psychiatric disorders and several mouse models of psychiatric diseases. Specifically, the hyperactivity may mirror the manic episodes in BD. To obtain a more physiological, long-term quantification of the hyperactive phenotype, we implanted nano tag® sensor chips in the animals, to enable the continuous monitoring of both activity and body temperature. During the light-off period, Pcdh15-null exhibited elevated activity and body temperature compared with wild-type (WT) mice. However, we observed a decreased body temperature during the light-on period. Comprehensive brain activity was visualized using c-Fos mapping, which was assessed during the activity and temperature peak and trough. There was a stark contrast between the distribution of c-Fos expression in Pcdh15-null and WT brains during both the light-on and light-off periods. These results provide valuable insights into the neural basis of the behavioral and thermal characteristics of Pcdh15-deletion mice. Therefore, Pcdh15-deletion mice can be a novel model for BD with mania and other psychiatric disorders, with a strong genetic component that satisfies both construct and surface validity.

Multidisciplinary analysis of cancer-related fatigue at the time of diagnosis: preliminary results of the BIOCARE FActory cohort.

Cancer-related fatigue (CRF) is a common side effect of cancer and cancer treatment that significantly impairs the quality of life and can persist for years after treatment completion. Although fatigue is often associated with cancer treatment, it is also a result of the disease itself, even before intervention. CRF at the time of diagnosis may affect treatment timing or completion and is a consistent predictor of post-treatment fatigue at any time. The mechanisms underlying CRF are multidimensional and not well understood, particularly at the time of diagnosis. Sixty-five breast cancer patients at the time of diagnosis were included. The participants completed self-assessment questionnaires about CRF, sleep disturbances, and emotional symptoms and wore an accelerometer to assess levels of spontaneous physical activity and sleep quality. During the experimental session, the participants underwent cognitive, neuromuscular, and exercise metabolism evaluations. Using augmented backward elimination regression, this study found that emotional symptoms and perceived sleep disturbances were the strongest predictors of CRF (adjusted r2 = 0.51). Neuromuscular fatigability and sleep disturbance were also associated with physical dimensions, whereas cognitive performance was associated with cognitive dimensions. At the time of diagnosis, emotional and cognitive dimensions are over-represented compared to the general population, and specific subdimensions have specific predictors that support the idea of distinct mechanisms. Evaluating CRF subdimensions and their potential mechanisms at the time of diagnosis would be particularly relevant for identifying high-risk patients and offering them appropriate interventions. This study was registered at ClinicalTrials.gov (NCT04391543) in May, 2020.

Self-esteem mediates the relationship between the parahippocampal gyrus and decisional procrastination at resting state.

When faced with a conflict or dilemma, we tend to postpone or even avoid making a decision. This phenomenon is known as decisional procrastination. Here, we investigated the neural correlates of this phenomenon, in particular the parahippocampal gyrus (PHG) that has previously been identified in procrastination studies. In this study, we applied an individual difference approach to evaluate participants' spontaneous neural activity in the PHG and their decisional procrastination levels, assessed outside the fMRI scanner. We discovered that the fractional amplitude of low-frequency fluctuations (fALFF) in the caudal PHG (cPHG) could predict participants' level of decisional procrastination, as measured by the avoidant decision-making style. Importantly, participants' self-esteem mediated the relationship between the cPHG and decisional procrastination, suggesting that individuals with higher levels of spontaneous activity in the cPHG are likely to have higher levels of self-esteem and thus be more likely to make decisions on time. In short, our study broadens the PHG's known role in procrastination by demonstrating its link with decisional procrastination and the mediating influence of self-esteem, underscoring the need for further exploration of this mediation mechanism.

A systematic review of altered resting-state networks in early deafness and implications for cochlear implantation outcomes.

Auditory deprivation following congenital/pre-lingual deafness (C/PD) can drastically affect brain development and its functional organisation. This systematic review intends to extend current knowledge of the impact of C/PD and deafness duration on brain resting-state networks (RSNs), review changes in RSNs and spoken language outcomes post-cochlear implant (CI) and draw conclusions for future research. The systematic literature search followed the PRISMA guideline. Two independent reviewers searched four electronic databases using combined keywords: 'auditory deprivation', 'congenital/prelingual deafness', 'resting-state functional connectivity' (RSFC), 'resting-state fMRI' and 'cochlear implant'. Seventeen studies (16 cross-sectional and one longitudinal) met the inclusion criteria. Using the Crowe Critical Appraisal Tool, the publications' quality was rated between 65.0% and 92.5% (mean: 84.10%), ≥80% in 13 out of 17 studies. A few studies were deficient in sampling and/or ethical considerations. According to the findings, early auditory deprivation results in enhanced RSFC between the auditory network and brain networks involved in non-verbal communication, and high levels of spontaneous neural activity in the auditory cortex before CI are evidence of occupied auditory cortical areas with other sensory modalities (cross-modal plasticity) and sub-optimal CI outcomes. Overall, current evidence supports the idea that moreover intramodal and cross-modal plasticity, the entire brain adaptation following auditory deprivation contributes to spoken language development and compensatory behaviours.

Switch from fight-flight to freeze-hide: The impacts of severe stress and brain serotonin on behavioral adaptations in flatfish.

Animals often experience changes in their environment that can be perceived as stressful. Previous evidence indicates that different individuals may have distinct stress responses. The role of serotonin (5-HT) in stress adaptation is well established, but its relationship with different defense strategies and the persistence of physiological and behavioral responses in different individuals during repeated acute stress remain unclear. In this study, using olive flounder (Paralichthys olivaceus) as a model, we analyzed the relationship between boldness and neurotransmitter 5-HT activity. We found that 5-HT suppression with 5-HT synthesis inhibitor p-chlorophenylalanine (pCPA) and 5-HT receptor subtype 1A (5-HT1A) antagonist WAY-100635 increased their oxygen consumption rates and the boldness of shy individuals. We determined the metabolic and behavioral changes in bold and shy individuals to repeated acute stress. The results suggest that bold individuals switch on passive "energy-saving" personality by changing their defense behavior from "fight-flight" to "freeze-hide" during a threat encounter, which manifests high behavioral plasticity. Both behavioral types decreased their spontaneous activity levels, which were also strengthened by limiting metabolic rate. Interestingly, treatment with pCPA and WAY-100635 before stress procedure attenuated stress and increased the boldness across diverse behavioral types. This study provides the initial empirical evidence of how perception of stress impacts both individual defense behavior and personality in this species. These findings can enhance our comprehension of individual variability and behavioral plasticity in animals, thereby improving our ability to develop effective adaptive management strategies.

Dynamic Design of 3D Structures in Indoor and Outdoor Spaces by Integrating Perceptual and Behavioral Correlation Methods

Abstract Redefining the intersection of user perception and spatial design, this research introduces a sophisticated design methodology that integrates quantitative visual perception analysis with user behavior insights to optimize spatial configurations. Conducted across 15 communities in City H, the study employs a mix of questionnaires and observational tactics to identify how design elements correlate with user engagement. Findings reveal that environmental qualities, such as tranquility and clear signage, alongside the density of fitness equipment, significantly affect residents’ activity patterns, with a notable correlation (R²=0.727) between equipment density and spontaneous activity levels. This method promises enhanced space efficiency and user satisfaction by weaving user feedback into the spatial design process, offering a novel paradigm for spatial design innovation.

Stochastic resonance in sparse neuronal network: functional role of ongoing activity to detect weak sensory input in awake auditory cortex of rat.

The awake cortex is characterized by a higher level of ongoing spontaneous activity, but it has a better detectability of weak sensory inputs than the anesthetized cortex. However, the computational mechanism underlying this paradoxical nature of awake neuronal activity remains to be elucidated. Here, we propose a hypothetical stochastic resonance, which improves the signal-to-noise ratio (SNR) of weak sensory inputs through nonlinear relations between ongoing spontaneous activities and sensory-evoked activities. Prestimulus and tone-evoked activities were investigated via in vivo extracellular recording with a dense microelectrode array covering the entire auditory cortex in rats in both awake and anesthetized states. We found that tone-evoked activities increased supralinearly with the prestimulus activity level in the awake state and that the SNR of weak stimulus representation was optimized at an intermediate level of prestimulus ongoing activity. Furthermore, the temporally intermittent firing pattern, but not the trial-by-trial reliability or the fluctuation of local field potential, was identified as a relevant factor for SNR improvement. Since ongoing activity differs among neurons, hypothetical stochastic resonance or "sparse network stochastic resonance" might offer beneficial SNR improvement at the single-neuron level, which is compatible with the sparse representation in the sensory cortex.

Does Spontaneous Physical Activity Level Determine Cognitive Benefits From The Environmental Enrichment?

Does Spontaneous Physical Activity Level Determine Cognitive Benefits From The Environmental Enrichment?

Creatine Supplementation Alleviates Fatigue after Exercise through Anti-Inflammatory Action in Skeletal Muscle and Brain

Eccentric exercise induces muscle damage and inflammation, resulting in a state of reduced physical activity with muscle dysfunction and a feeling of tiredness after exercise. Creatine is known to act as an energy buffer, but it has also been suggested to exert inhibitory effects on muscle damage and peripheral inflammation. The purpose of this study was to test the hypothesis that creatine supplementation alleviates fatigue after eccentric exercise and to explore the mechanism of this effect. C57BL/6J mice were fed an AIN-93G-formulated control diet or a creatine-containing diet for 6 days and were then subjected to downhill running, a model of eccentric exercise, to assess the effects on the total creatine concentrations in skeletal muscle and brain tissue, spontaneous activity, the urine concentration of titin N-fragment, and inflammatory gene expression. The results showed that creatine supplementation significantly increased the total creatine concentrations in skeletal muscle and brain tissue. Furthermore, spontaneous activity significantly decreased after downhill running and creatine supplementation maintained a significantly higher level of spontaneous activity. In addition, creatine supplementation significantly suppressed the downhill-running-induced increase in the mRNA expression of genes encoding ICAM-1, E-selectin, CD18, and BKB1R in the soleus muscle and IL-1β in the hypothalamus. On the other hand, creatine supplementation did not clearly influence the urine concentration of titin N-fragment. These results indicate that creatine supplementation may alleviate fatigue after eccentric exercise by partially suppressing inflammation in slow-twitch skeletal muscle and brain tissue.

Reduced levels of NGF shift astrocytes toward a neurotoxic phenotype.

Nerve growth factor (NGF) is critical for neuronal physiology during development and adulthood. Despite the well-recognized effect of NGF on neurons, less is known about whether NGF can actually affect other cell types in the central nervous system (CNS). In this work, we show that astrocytes are susceptible to changes in ambient levels of NGF. First, we observe that interfering with NGF signaling in vivo via the constitutive expression of an antiNGF antibody induces astrocytic atrophy. A similar asthenic phenotype is encountered in an uncleavable proNGF transgenic mouse model (TgproNGF#72), effectively increasing the brain proNGF levels. To examine whether this effect on astrocytes is cell-autonomous, we cultured wild-type primary astrocytes in the presence of antiNGF antibodies, uncovering that a short incubation period is sufficient to potently and rapidly trigger calcium oscillations. Acute induction of calcium oscillations by antiNGF antibodies is followed by progressive morphological changes similar to those observed in antiNGF AD11 mice. Conversely, incubation with mature NGF has no effect on either calcium activity nor on astrocytic morphology. At longer timescales, transcriptomic analysis revealed that NGF-deprived astrocytes acquire a proinflammatory profile. In particular, antiNGF-treated astrocytes show upregulation of neurotoxic transcripts and downregulation of neuroprotective mRNAs. Consistent with that data, culturing wild-type neurons in the presence of NGF-deprived astrocytes leads to neuronal cell death. Finally, we report that in both awake and anesthetized mice, astrocytes in layer I of the motor cortex respond with an increase in calcium activity to acute NGF inhibition using either NGF-neutralizing antibodies or a TrkA-Fc NGF scavenger. Moreover, in vivo calcium imaging in the cortex of the 5xFAD neurodegeneration mouse model shows an increased level of spontaneous calcium activity in astrocytes, which is significantly reduced after acute administration of NGF. In conclusion, we unveil a novel neurotoxic mechanism driven by astrocytes, triggered by their sensing and reacting to changes in the levels of ambient NGF.

Spontaneous neurotransmission at evocable synapses predicts their responsiveness to action potentials.

Synaptic transmission relies on presynaptic neurotransmitter (NT) release from synaptic vesicles (SVs) and on NT detection by postsynaptic receptors. Transmission exists in two principal modes: action-potential (AP) evoked and AP-independent, "spontaneous" transmission. AP-evoked neurotransmission is considered the primary mode of inter-neuronal communication, whereas spontaneous transmission is required for neuronal development, homeostasis, and plasticity. While some synapses appear dedicated to spontaneous transmission only, all AP-responsive synapses also engage spontaneously, but whether this encodes functional information regarding their excitability is unknown. Here we report on functional interdependence of both transmission modes at individual synaptic contacts of Drosophila larval neuromuscular junctions (NMJs) which were identified by the presynaptic scaffolding protein Bruchpilot (BRP) and whose activities were quantified using the genetically encoded Ca2+ indicator GCaMP. Consistent with the role of BRP in organizing the AP-dependent release machinery (voltage-dependent Ca2+ channels and SV fusion machinery), most active BRP-positive synapses (>85%) responded to APs. At these synapses, the level of spontaneous activity was a predictor for their responsiveness to AP-stimulation. AP-stimulation resulted in cross-depletion of spontaneous activity and both transmission modes were affected by the non-specific Ca2+ channel blocker cadmium and engaged overlapping postsynaptic receptors. Thus, by using overlapping machinery, spontaneous transmission is a continuous, stimulus independent predictor for the AP-responsiveness of individual synapses.

Integrating functional neuroimaging and serum proteins improves the diagnosis of major depressive disorder

BackgroundThe lack of effective objective diagnostic biomarkers for major depressive disorder (MDD) leads to high misdiagnosis. Compared with healthy controls (HC), abnormal brain functions and protein levels are often observed in MDD. However, it is unclear whether combining these changed multidimensional indicators could help improve the diagnosis of MDD. MethodsSixty-three MDD and eighty-one HC subjects underwent resting-state fMRI scans, among whom 37 MDD and 45 HC provided blood samples. Amplitudes of low-frequency fluctuation (ALFF), regional homogeneity (ReHo), and serum levels of brain-derived neurotrophic factor (BDNF), cortisol, and multiple cytokines were measured and put into the linear discriminant analysis (LDA) to construct corresponding MDD diagnostic models. The area under the receiver operating characteristic curve (AUC) of 5-fold cross-validation was calculated to evaluate each model's performance. ResultsCompared with HC, MDD patients' spontaneous brain activity, serum BDNF, cortisol, interleukin (IL)-4, IL-6, and IL-10 levels changed significantly. The combinations of unidimensional multi-indicator had better diagnostic performance than a single one. The model consisted of multidimensional multi-indicator further exhibited conspicuously superior diagnostic efficiency than those constructed with unidimensional multi-indicator, and its AUC, sensitivity, specificity, and accuracy of 5-fold cross-validation were 0.99, 92.0 %, 100.0 %, and 96.3 %, respectively. LimitationsThis cross-sectional study consists of relatively small samples and should be replicated in larger samples with follow-up data to optimize the diagnostic model. ConclusionsMDD patients' neuroimaging features and serum protein levels significantly changed. The model revealed by LDA could diagnose MDD with high accuracy, which may serve as an ideal diagnostic biomarker for MDD.

Synapse integrity and function: Dependence on protein synthesis and identification of potential failure points.

Synaptic integrity and function depend on myriad proteins - labile molecules with finite lifetimes that need to be continually replaced with freshly synthesized copies. Here we describe experiments designed to expose synaptic (and neuronal) properties and functions that are particularly sensitive to disruptions in protein supply, identify proteins lost early upon such disruptions, and uncover potential, yet currently underappreciated failure points. We report here that acute suppressions of protein synthesis are followed within hours by reductions in spontaneous network activity levels, impaired oxidative phosphorylation and mitochondrial function, and, importantly, destabilization and loss of both excitatory and inhibitory postsynaptic specializations. Conversely, gross impairments in presynaptic vesicle recycling occur over longer time scales (days), as does overt cell death. Proteomic analysis identified groups of potentially essential 'early-lost' proteins including regulators of synapse stability, proteins related to bioenergetics, fatty acid and lipid metabolism, and, unexpectedly, numerous proteins involved in Alzheimer's disease pathology and amyloid beta processing. Collectively, these findings point to neuronal excitability, energy supply and synaptic stability as early-occurring failure points under conditions of compromised supply of newly synthesized protein copies.

Differential axonal trafficking of Neuropeptide Y-, LAMP1-, and RAB7-tagged organelles in vivo.

Different organelles traveling through neurons exhibit distinct properties in vitro, but this has not been investigated in the intact mammalian brain. We established simultaneous dual color two-photon microscopy to visualize the trafficking of Neuropeptide Y (NPY)-, LAMP1-, and RAB7-tagged organelles in thalamocortical axons imaged in mouse cortex in vivo. This revealed that LAMP1- and RAB7-tagged organelles move significantly faster than NPY-tagged organelles in both anterograde and retrograde direction. NPY traveled more selectively in anterograde direction than LAMP1 and RAB7. By using a synapse marker and a calcium sensor, we further investigated the transport dynamics of NPY-tagged organelles. We found that these organelles slow down and pause at synapses. In contrast to previous in vitro studies, a significant increase of transport speed was observed after spontaneous activity and elevated calcium levels in vivo as well as electrically stimulated activity in acute brain slices. Together, we show a remarkable diversity in speeds and properties of three axonal organelle marker in vivo that differ from properties previously observed in vitro.

Relationship between Adenosine Deaminase Activity in the Cerebral Cortex and the Stimulating Effect of Caffeine in Adult Wistar Rats of Different Ages.

The aim of this study was to test the hypothesis that the higher the activity of adenosinedeaminase (ADA) in the brain, the greater should be the motor activity of animals, and possibly the stronger the psychostimulant effect of caffeine. We studied the effect of caffeine (10 and 20 mg/kg) on the motor activity and ADA activity in the frontal cortex of the brain in 2- and 5-month-old rats with different levels of spontaneous motor activity. Total motor activity significantly decreased with age, which was accompanied by a decrease in ADA activity. Administration of caffeine in a dose of 10 mg/kg stimulated motor activity in both 2- and 5-month-old animals, while ADA activity decreased in 2-month-old rats and increased in 5-month-old animals. Administration of caffeine in a dose of 20 mg/kg did not change the motor activity, however, in 5-month-old animals it led to an even greater increase in ADA activity. Thus, the age-related decrease in motor activity can be due to a decrease in ADA activity. However, the effect of caffeine on motor activity is not directly related to ADA activity in the cerebral cortex.

Neurophysiological Effects of the Anterior Cingulate Cortex on the Exacerbation of Crohn's Disease: A Combined fMRI-MRS Study.

BackgroundCrohn’s disease (CD) is characterized by repetitive phases of remission and exacerbation, the quality of life of patients with CD is strongly influenced by disease activity, as patients in the active phase experience significantly worse symptoms. To investigate the underlying mechanism of how the course of CD is exacerbated based on the bi-directionality of the brain-gut axis (BGA), we conducted a multi-modality neuroimaging study that combined resting-state functional magnetic resonance imaging (rs-fMRI) with proton magnetic resonance spectroscopy (MRS) to detect abnormalities in the anterior cingulate cortex (ACC).Materials and MethodsClinical scales including Visual Analog Scale (VAS) and Hospital Anxiety and Depression Scale (HADS) were used to evaluate the degree of abdominal pain and mood state of participants. We made a comparison between CD patients in the active phase, the remission phase and healthy controls (HCs), not only employed the innovative wavelet-transform to analyze the amplitude of low frequency fluctuation (ALFF) but also compared the sensitivity of wavelet-transform and the traditional fast Fourier transform (FFT). Brain metabolites such as glutamate (Glu), myo-inositol (mIns) and gamma-aminobutyric acid (GABA) were also detected. Then correlation analysis was made to see whether changes in the ACC correlated with CD’s clinical symptoms.ResultsCD patients in the active phase showed higher VAS scores (p = 0.025), the scores of anxiety and depression were also higher (all p < 0.05). Wavelet-transform is slightly more sensitive in the current research. Patients in the active phase exhibited higher ALFF in the left ACC and the left superior frontal gyrus, medial (SFGmed). Patients in the active phase showed increased Glu levels in the ACC than patients in the remission phase or HCs (p = 0.039 and 0.034 respectively) and lower levels of mIns than HCs (p = 0.036). There was a positive correlation between mWavelet-ALFF values of the ACC and HADS-depression scores in CD patients (r = 0.462, p = 0.006). Besides, concentrations of Glu positively correlated with mWavelet-ALFF in the ACC in all participants (r = 0.367, p = 0.006).ConclusionAbnormal spontaneous activity and metabolic levels in the ACC were detected in CD patients in the active phase along with severer abdominal pain and worse mood state, these may contribute to the exacerbation of CD. Therefore, the ACC might be a potential neural alternative for managing the exacerbation of CD.

An increase in spontaneous activity mediates visual habituation.

SUMMARYThe cerebral cortex is spontaneously active, but the function of this ongoing activity remains unclear. To test whether spontaneous activity encodes learned experiences, we measured the response of neuronal populations in mouse primary visual cortex with chronic two-photon calcium imaging during visual habituation to a specific oriented stimulus. We find that, during habituation, spontaneous activity increases in neurons across the full range of orientation selectivity, eventually matching that of evoked levels. This increase in spontaneous activity robustly correlates with the degree of habituation. Moreover, boosting spontaneous activity with two-photon optogenetic stimulation to the levels of visually evoked activity accelerates habituation. Our study shows that cortical spontaneous activity is linked to habituation, and we propose that habituation unfolds by minimizing the difference between spontaneous and stimulus-evoked activity levels. We conclude that baseline spontaneous activity could gate incoming sensory information to the cortex based on the learned experience of the animal.

The Impact of Sparse Coding on Memory Lifetimes in Simple and Complex Models of Synaptic Plasticity

Models of associative memory with discrete state synapses learn new memories by forgetting old ones. In the simplest models, memories are forgotten exponentially quickly. Sparse population coding ameliorates this problem, as do complex models of synaptic plasticity that posit internal synaptic states, giving rise to synaptic metaplasticity. We examine memory lifetimes in both simple and complex models of synaptic plasticity with sparse coding. We consider our own integrative, filter-based model of synaptic plasticity, and examine the cascade and serial synapse models for comparison. We explore memory lifetimes at both the single-neuron and the population level, allowing for spontaneous activity. Memory lifetimes are defined using either a signal-to-noise ratio (SNR) approach or a first passage time (FPT) method, although we use the latter only for simple models at the single-neuron level. All studied models exhibit a decrease in the optimal single-neuron SNR memory lifetime, optimised with respect to sparseness, as the probability of synaptic updates decreases or, equivalently, as synaptic complexity increases. This holds regardless of spontaneous activity levels. In contrast, at the population level, even a low but nonzero level of spontaneous activity is critical in facilitating an increase in optimal SNR memory lifetimes with increasing synaptic complexity, but only in filter and serial models. However, SNR memory lifetimes are valid only in an asymptotic regime in which a mean field approximation is valid. By considering FPT memory lifetimes, we find that this asymptotic regime is not satisfied for very sparse coding, violating the conditions for the optimisation of single-perceptron SNR memory lifetimes with respect to sparseness. Similar violations are also expected for complex models of synaptic plasticity.