Behavioural Brain Research最新文献

{"title":"A novel analysis of interoceptive underpinnings of anxious psychopathology in COVID-19 survivors","authors":"Greta D’Orsi ,&nbsp;Mariagrazia Palladini ,&nbsp;Mario Gennaro Mazza ,&nbsp;COVID-19 BioB Outpatient Clinic Study group,&nbsp;Patrizia Rovere-Querini ,&nbsp;Andrea Scalabrini ,&nbsp;Francesco Benedetti","doi":"10.1016/j.bbr.2024.115275","DOIUrl":"10.1016/j.bbr.2024.115275","url":null,"abstract":"<div><h3>Introduction</h3><div>SARS-CoV-2 affects brain, body, and their interchange. We investigated interoceptive mechanisms in COVID-19 survivors focusing on their potential link with psychopathology and inflammatory biomarkers.</div></div><div><h3>Methods</h3><div>We assessed interoceptive accuracy (IAc) and time-perceiving (TA) skills of 57 COVID-19 survivors one month after hospital discharge through, respectively, a heartbeats perception task and a time duration task. Each participant was assessed about his interoceptive awareness (IAw) through Multidimensional Assessment of Interoceptive Awareness questionnaire (MAIA) and then, screened for post-traumatic (Impact of Events Scale – IES-R), anxious (State-Trait Anxiety Inventory – STAI-Y1) and depressive (Zung Self-Rating Depression Scale - ZSDS; Beck Depression Inventory - BDI-13) symptoms.</div><div>Biomarkers of inflammation (platelet count, PC; mean platelet volume, MPV and systemic immune-inflammation index, SII) were obtained in a subsample of 40 survivors by a blood sampling conducted at admission and discharge time from the hospital. Correlational, GLM, GLMZ, and mediation analyses were performed.</div></div><div><h3>Results</h3><div>IAc did not correlate with TA confirming the reliability of interoceptive measure. IAc positively predicts MAIA’s Trusting subscale and negatively predicts anxious psychopathology which fully mediates the effect of IAc on Trusting.PC at hospital admission predicts anxiety at one month after recovery. Again, a higher decrease of SII during hospitalization predicts higher IAc skill and lower anxiety state at one month. The link between SII change and anxiety is fully mediated by IAc.</div></div><div><h3>Conclusions</h3><div>Our results unveil a potential key role of interoception and brain-body interchange in the exacerbation and maintenance of anxiety psychopathology in COVID-19 survivors.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurodegeneration: Effects of calorie restriction on the brain sirtuin protein levels","authors":"Basar Atalay ,&nbsp;Soner Dogan ,&nbsp;Burhan Oral Gudu ,&nbsp;Elif Yilmaz ,&nbsp;Atakan Ayden ,&nbsp;Umit Ozorhan ,&nbsp;Munevver Burcu Cicekdal ,&nbsp;Kaan Yaltirik ,&nbsp;Isin Dogan Ekici ,&nbsp;Bilge Guvenc Tuna","doi":"10.1016/j.bbr.2024.115258","DOIUrl":"10.1016/j.bbr.2024.115258","url":null,"abstract":"<div><h3>Background</h3><div>Calorie restriction (CR) is suggested to activate protective mechanisms in neurodegenerative diseases (NDDs). Despite existing literature highlighting the protective role of Sirtuin (SIRT) proteins against age-related neurodegeneration (ND), no study has explored the total levels of SIRT 1, 3, and 6 proteins simultaneously in brain homogenates by ELISA following intermittent calorie restriction. Applying CR protocols in mice to induce stress, we aimed to determine whether ND would be more pronounced with ad libitum (AL) or with CR.</div></div><div><h3>Methods</h3><div>Mice were randomly assigned to ad libitum (AL), Chronic CR (CCR), or Intermittent CR (ICR) groups at 10 weeks of baseline age (BL). SIRT 1, 3, and 6 protein levels were measured in the homogenized whole-brain supernatants of 49/50 weeks old mice by the ELISA method. Neuronal morphology was evaluated by the cresyl violet on the hippocampus. Neurodegeneration (ND) was assessed by the fluoro-jade and ImageJ was used for quantifications.</div></div><div><h3>Results</h3><div>In the ICR group, SIRT1 levels were elevated compared to both the AL and BL groups. Similarly, the CCR group exhibited higher SIRT1 values compared to the AL and BL groups. While SIRT3 levels were higher in both the ICR and CCR groups compared to the AL and BL groups, this disparity did not reach statistical significance. SIRT6 levels were also higher in the ICR group compared to both the BL and AL groups, with the CCR group showing higher values compared to the BL and AL groups as well. Image quantification demonstrated significant neurodegeneration in the AL group compared to the CCR and ICR group, with no observed alterations in nerve cell morphology and number.</div></div><div><h3>Conclusion</h3><div>This study revealed that the levels of SIRT 1, SIRT 3, and SIRT 6 in brain tissue were notably elevated, and there was less evidence of ND at the 50-week mark in groups undergoing continuous calorie restriction and intermittent calorie restriction compared to baseline and ad libitum groups. Our findings illustrate that CR promotes increased SIRT expression in the mouse brain, thereby potentially mitigating neurodegeneration.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural mechanisms of cooperation and fairness in iterative prisoner’s dilemma","authors":"Xizhuo Zou ,&nbsp;Dandan Li ,&nbsp;Ofir Turel ,&nbsp;Qinghua He","doi":"10.1016/j.bbr.2024.115272","DOIUrl":"10.1016/j.bbr.2024.115272","url":null,"abstract":"<div><div>Cooperation is a universal human principle reflecting working with others to achieve common goals. The rational decision-making model contends that cooperation is the best strategy for maximizing benefits in an iterative prisoner’s dilemma. However, the motivations for cooperation (or betrayal) are complex and diverse, and often include fairness reflections. In this study, we used functional magnetic resonance imaging to study underlying neural differences in brain regions related to fairness when people interact with an opponent who tend to cooperate or betray, at different decision-making stages. Results based on 40 university students (25 women) indicate that experiences of cooperation or betrayal affect people’s fairness perception. Distinct neural activities occur in expectation, decision, and outcome phases of decisions. In the expectation phase, those in the cooperative condition exhibited increased activation in the anterior cingulate gyrus, medial superior frontal gyrus, and caudate nucleus compared to those in the uncooperative condition. During the decision phase, those in the cooperative condition showed greater activation in the middle frontal gyrus, caudate nucleus/frontal insula, inferior frontal gyrus, and cingulate gyrus compared to those in the uncooperative condition. In the outcome feedback phase, the caudate nucleus, insula, cingulate gyrus, and inferior frontal gyrus of the orbit were more active in the uncooperative condition than in the cooperative condition. Results also showed a significant correlation between caudate activity and the perception of fairness when expecting uncooperative conditions.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"(2R, 6R)-hydroxynorketamine ameliorates PTSD-like behaviors during the reconsolidation phase of fear memory in rats by modulating the VGF/BDNF/GluA1 signaling pathway in the hippocampus","authors":"Han Wang ,&nbsp;Yuxuan He ,&nbsp;Jiahao Tang ,&nbsp;Yang Liu ,&nbsp;Chunyan Wu ,&nbsp;Changjiang Li ,&nbsp;Hongwei Sun ,&nbsp;Lin Sun","doi":"10.1016/j.bbr.2024.115273","DOIUrl":"10.1016/j.bbr.2024.115273","url":null,"abstract":"<div><h3>Rationale</h3><div>Fear memory, a fundamental symptom of post-traumatic stress disorder (PTSD), is improved by (2R, 6R)-hydroxynorketamine ((2R, 6R)-HNK) administration. However, the phase of fear memory in which the injected drug is the most effective at mitigating PTSD-like effects remains unknown.</div></div><div><h3>Objective</h3><div>This study aimed to explore the effects of (2 R, 6 R)-HNK administration during three phases [acquisition (AP), reconsolidation (RP), and extinction (EP)] on PTSD-like behaviors in single prolonged stress (SPS) and contextual fear conditioning (CFC) rat models. The effects of VGF-inducible type of nerve growth factor (VGF), brain-derived neurotrophic factor (BDNF), and GluA1 on hippocampus (HIP) expression were also explored.</div></div><div><h3>Methods</h3><div>SPS and CFC (SPSC) were used to establish a PTSD rat model. After lateral ventricle injection of 5 μL (2 R, 6 R)-HNK (0.5 nmol). Anxiety-depression-like behaviors were assessed in rats by the open field test (OFT) and elevated plus maze test (EPMT). Situational fear responses were evaluated in rodents by freezing behavior test (FBT) test. In addition, GluA1, VGF, and BDNF were assessed in the hippocampus by Western blot assay (WB) and Immunohistochemistry assay (IF).</div></div><div><h3>Results</h3><div>SPSC procedure induced PTSD-like behaviors. The SPSC group had decreased spontaneous exploratory behavior and increased fear response. The (2R, 6R)-HNK group showed improved SPSC-induced reduction in GluA1, VGF, and BDNF levels in the HIP. During RP, anxiety and fear avoidance behaviors were alleviated, and the protein levels of GluA1, VGF, and BDNF in the HIP were restored. In contrast, no significant improvement was noted during AP and EP.</div></div><div><h3>Conclusions</h3><div>(2R,6R)-HNK modulates the VGF/BDNF/GluA1 signaling pathway in the hippocampus and improves PTSD-like behaviors during the reconsolidation phase of fear memory in rats, which may provide a new target for the clinical treatment and prevention of fear-related disorders such as PTSD.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic brain entropy predicts risky decision-making across transdiagnostic dimensions of psychopathology","authors":"Shanling Ji ,&nbsp;Fujian Chen ,&nbsp;Sen Li ,&nbsp;Cong Zhou ,&nbsp;Chuanxin Liu ,&nbsp;Hao Yu","doi":"10.1016/j.bbr.2024.115255","DOIUrl":"10.1016/j.bbr.2024.115255","url":null,"abstract":"<div><h3>Objectives</h3><div>Maladaptive risky decision-making is a common pathological behavior among patients with various psychiatric disorders. Brain entropy, which measures the complexity of brain time series signals, provides a novel approach to assessing brain health. Despite its potential, the dynamics of brain entropy have seldom been explored. This study aimed to construct a dynamic model of brain entropy and examine its predictive value for risky decision-making in patients with mental disorders, utilizing resting-state functional magnetic resonance imaging (rs-fMRI).</div></div><div><h3>Methods</h3><div>This study analyzed the rs-fMRI data from a total of 198 subjects, including 48 patients with bipolar disorder (BD), 47 patients with schizophrenia (SZ), 40 patients with adult attention deficit hyperactivity disorder (ADHD), as well as 63 healthy controls (HC). Time series signals were extracted from 264 brain regions based on rs-fMRI. The traditional static entropy and dynamic entropy (coefficient of variation, CV; rate of change, Rate) were constructed, respectively. Support vector regression was employed to predict risky decision-making utilizing leave-one-out cross-validation within each group.</div></div><div><h3>Results</h3><div>Our findings showed that CV achieved the best performances in HC and BD groups (r = −0.58, MAE = 6.43, R² = 0.32; r = −0.78, MAE = 12.10, R² = 0.61), while the Rate achieved the best in SZ and ADHD groups (r = −0.69, MAE = 10.20, R² = 0.47; r = −0.78, MAE = 7.63, R² = 0.60). For the dynamic entropy, the feature selection threshold rather than the time window length and overlapping ratio influenced predictive performance.</div></div><div><h3>Conclusions</h3><div>These results suggest that dynamic brain entropy could be a more effective predictor of risky decision-making than traditional static brain entropy. Our findings offer a novel perspective on exploring brain signal complexity and can serve as a reference for interventions targeting risky decision-making behaviors, particularly in individuals with psychiatric diagnoses.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142318770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Remimazolam attenuates lipopolysaccharide-induced neuroinflammation and cognitive dysfunction","authors":"Leguang Zhou ,&nbsp;Hongzhao Shi ,&nbsp;Mengzhe Xiao ,&nbsp;Wenjie Liu ,&nbsp;Lijuan Wang ,&nbsp;Shangtao Zhou ,&nbsp;Shenghua Chen ,&nbsp;Yan Wang ,&nbsp;Chengxi Liu","doi":"10.1016/j.bbr.2024.115268","DOIUrl":"10.1016/j.bbr.2024.115268","url":null,"abstract":"<div><h3>Objective</h3><div>Remimazolam, a novel benzodiazepine, is widely used as an anesthetic in endoscopic procedures; however<u><u>,</u></u> its effects on cognitive function remain unclear, limiting its broader application in general anaesthesia. Neuroinflammation is a well-established key factor in the etiology and progression of cognitive dysfunction, including conditions such as Alzheimer's disease, Parkinson's disease, postoperative delirium, and postoperative cognitive dysfunction. Preclinical studies have demonstrated that remimazolam exerts anti-inflammatory and neuroprotective effects, and clinical reports indicate a reduced incidence of postoperative delirium in patients treated with remimazolam. Nevertheless, whether remimazolam improves cognitive function through its anti-inflammatory properties remains uncertain. This study aimed to investigate the neuroprotective effects of remimazolam and its underlying mechanism in a lipopolysaccharide (LPS)-induced model of neuroinflammation, neuronal injury, and cognitive dysfunction</div></div><div><h3>Methods</h3><div>C57BL/6 J male mice were administered LPS intraperitoneally to establish a model of neuroinflammation-induced cognitive impairment. A subset of mice received remimazolam via intraperitoneal injection 30 minutes prior to LPS administration. Cognitive performance was evaluated using behavioural tests, including the Morris Water Maze (MWM), Novel Object Recognition (NOR) test, and Open Field Test (OFT). Hippocampal tissues were analyzed by haematoxylin-eosin (HE) staining to assess structural changes. Inflammatory markers, including Interleukin (IL)-6, IL-1β, and tumor necrosis factor-α, were quantified using enzyme-linked immunosorbent assay (ELISA) and real-time quantitative PCR. Immunofluorescence was used to detect translocator protein (TSPO) and markers of microglia activation (IBA-1, CD16/32, and CD206).</div></div><div><h3>Results</h3><div>(1) Remimazolam reversed LPS-induced cognitive deficits, as evidenced by shorter spatial exploration latency and increased platform crossings in the MWM, and an elevated recognition index in the NOR test. (2) Remimazolam improved hippocampal morphology, reducing LPS-induced neuronal damage. (3) Remimazolam significantly decreased levels of hippocampal inflammatory cytokines, inhibited microglial activation, promoted M2-type microglia polarization, and increased TSPO expression.</div></div><div><h3>Conclusion</h3><div>Remimazolam demonstrated neuroprotective and anti-neuroinflammatory effects in a mouse model of LPS-induced cognitive impairment. These effects are likely mediated through the regulation of TSPO, which inhibits microglial activation and promotes the polarization of microglia from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the association between common functional Nuclear Factor Kappa-b gene polymorphisms (NFKB1, NFKBIZ, NFKBIA) and Alzheimer´s disease","authors":"Daniel Vazquez-Coto ,&nbsp;Sergio Perez-Oliveira ,&nbsp;Manuel Menéndez-González ,&nbsp;Eliecer Coto ,&nbsp;Victoria Álvarez","doi":"10.1016/j.bbr.2024.115264","DOIUrl":"10.1016/j.bbr.2024.115264","url":null,"abstract":"<div><div>The Nuclear Factor Kappa-b (NF-Κb) pathway has been implicated in the pathogenesis of Alzheimer´s disease (AD). We determined whether common variants in the NF-Κb genes were associated with the risk of developing late-onset AD (LOAD). A total of 639 Spanish LOAD and 500 controls were genotyped for the <em>NFKB1</em> rs28362491/rs7667496, <em>NFKBIA</em> rs696, <em>NFKBIZ</em> rs3217713 and <em>APOE-Ɛ2/3/4</em> polymorphisms. Rs7667496 C was increased in the patients (p&lt;0.001) with the CC genotype showing a significant risk (CC vs T+, OR= 1.58, 95 %CI=1.25–2.01). The CC genotype was significantly associated with LOAD after correction by APOE-4+ genotypes, age and sex (p=0.0003, OR=1.88, 95 %CI=1.28–2.78). The <em>NFKB1</em> rs28362491 I - rs7667496 C haplotype was significantly increased in the patients (p=0.02). <em>NFKBIA</em> and <em>NFKBIZ</em> variants were not associated with the risk of LOAD in our population. In conclusion, <em>NFKB1</em> variants were associated with the risk of LOAD in our population. This finding encourages further studies to determine the involvement of the NF-kB components in LOAD.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel insights into famotidine as a GSK-3β inhibitor: An explorative study in aluminium chloride-induced Alzheimer’s disease rat model","authors":"Ronnita C. Sequeira ,&nbsp;Angel Godad","doi":"10.1016/j.bbr.2024.115270","DOIUrl":"10.1016/j.bbr.2024.115270","url":null,"abstract":"<div><div>Alzheimer's disease (AD), a chronic neurodegenerative disease, presents a substantial global health challenge. This study explored the potential therapeutic role of famotidine, a histamine (H2) receptor antagonist, as a glycogen synthase kinase-3β (GSK-3β) inhibitor in the context of AD induced by aluminium chloride (AlCl₃) in a rat model. The intricate relationship between GSK-3β dysregulation and AD pathogenesis, particularly in amyloid-β (Aβ) production, formed the basis for investigating famotidine's efficacy. Molecular modelling revealed famotidine's efficient binding to GSK-3β, suggesting inhibitory potential. In behavioural assessments, famotidine-treated groups exhibited dose-dependent improvements in Morris Water Maze, Novel Object Recognition, and Y-Maze tests, comparable to the standard Rivastigmine tartrate group. Biochemical analyses showed that famotidine inhibits acetylcholinesterase, decreases lipid peroxidation, increases antioxidant activity, and mitigates oxidative stress. Moreover, famotidine significantly lowered the levels of GSK-3β, IL-6, and Aβ(1−42). The neuroprotective effects of famotidine were further supported by histopathological analysis. This comprehensive investigation underscores famotidine's potential as a GSK-3β inhibitor, providing insights into its therapeutic impact on AD induced by AlCl₃. The study offers a promising avenue for repurposing famotidine due to its established safety profile and widespread availability, highlighting its potential in addressing the formidable challenge of AD.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The brain extracellular space in chronic kidney disease","authors":"Veronica Buonincontri ,&nbsp;Davide Viggiano ,&nbsp;Giuseppe Gigliotti ,&nbsp;for the Alzheimer’s Disease Neuroimaging Initiative","doi":"10.1016/j.bbr.2024.115271","DOIUrl":"10.1016/j.bbr.2024.115271","url":null,"abstract":"<div><div>The brain extracellular space (ECS) is a highly complex structure between the innumerable and intermingled processes of brain cells (neurons and glial cells). This space represents up to 20 % of total brain volume (excluding the ventricles) and hosts an extracellular matrix of proteoglycans. The regulation of this space is unclear, though it may differ from other organs due to the presence of the blood brain barrier. Changes in the ECS may modify the diffusion timing of volume-dependent neurotransmitters such as dopamine, thus potentially altering most brain activities. Indeed, recently it has been shown that mild cognitive impairment is correlated to a reduction of ECS. Because water and electrolyte homeostasis are tightly regulated by the kidney, it is possible that a reduced kidney filtration may change the brain extracellular space and therefore explain the reduced cognitive functions exhibited during kidney diseases. The present communication explores the regulation of ECS in the presence of kidney diseases, discussing how reduced kidney function might impact on brain structure and function in both mice and humans, and suggests potential mechanisms for this link.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142318771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The inhibitory control deficit of internet gaming disorder: An Event-Related Potentials(ERPs) study","authors":"Junjian Yu ,&nbsp;Mohammad Farris Iman Leong Bin Abdullah ,&nbsp;Nor Shuhada Mansor","doi":"10.1016/j.bbr.2024.115253","DOIUrl":"10.1016/j.bbr.2024.115253","url":null,"abstract":"<div><h3>Introduction</h3><div>The primary difficulty and challenge encountered by individuals with Internet Gaming Disorder (IGD) is inhibitory control deficit. Given that different types of inhibitory control have different effects on IGD patients, it is critical to investigate the neurological cognitive processes underlying various inhibitory control problems.</div></div><div><h3>Methods</h3><div>The IGD-20 questionnaire was used to identify Internet game disorder and healthy control group, and finally Internet game disorder in (<em>n</em>=25) and healthy control group (<em>n</em>=28) in Flanker task, Internet game disorder (<em>n</em>=29) and health control group (<em>n</em>=24) in GO/NOGO task. The Flanker task was employed to investigate distractor interference inhibition control in those with IGD, while the Go/NoGo task was used to measure their prepotent response inhibitory control. Event-related potentials (ERPs) were used to evaluate the brain mechanisms difference of both IGD and healthy participants during these different inhibitory control tasks.</div></div><div><h3>Results</h3><div>Findings indicate that compared to healthy control subjects, individuals with Internet Gaming Disorder (IGD) have deficits in inhibitory control tasks during both distraction inhibition and prepotent response inhibition tasks, and distraction inhibition occurs earlier than prepotent response inhibition. In distraction inhibition tasks, the IGD group's N2 amplitude is significantly lower than the healthy control groups. In prepotent response inhibition, the N2 amplitude provoked in the IGD group is not only significantly lower than in the healthy control group, but the P3 amplitude is also significantly larger in the IGD group. The main brain activity areas of interference inhibitory control are the frontal lobe and prefrontal lobe, while the main brain activity areas of prepotent response inhibitory control are the frontal lobe and occipital lobe.</div></div><div><h3>Conclusion</h3><div>The present study concentrates on the differential neurophysiological characteristics observed in individuals with Internet gaming problems, notably the ability to avoid distractions and prepotent reactions. The current research provides foundations for the assessment and development of tailored therapy and treatment methods to address the wide variety of cognitive problems reported in individuals with Internet Gaming Disorder (IGD).</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}