IBRO Neuroscience Reports最新文献

{"title":"Effects of ethanol exposure in neonatal mice on retinoic acid signaling in forebrain neurons and astrocytes","authors":"Mariko Saito ,&nbsp;Jungann Park ,&nbsp;Anusha Nalluri ,&nbsp;Brandon Marino ,&nbsp;Colin R.O. Williams ,&nbsp;Donald A. Wilson ,&nbsp;Bhaskar C. Das ,&nbsp;John F. Smiley","doi":"10.1016/j.ibneur.2026.05.006","DOIUrl":"10.1016/j.ibneur.2026.05.006","url":null,"abstract":"<div><div>Toxicity of prenatal ethanol leading to fetal alcohol spectrum disorders (FASDs) has been linked to disturbances in retinoic acid (RA) signaling necessary for embryonic development. While ethanol exposure in the postnatal day 7 (P7) mice, which induces immediate neurodegeneration and long-lasting GABAergic cell loss and behavioral deficits, has been used for the third trimester FASD model, involvement of RA signaling in the process has not been well explored. Using RARE-LacZ reporter mice that express β-galactosidase (β-Gal) under the control of retinoic acid response element (RARE), we examined RA signaling activity of the forebrains of P8 and P30 mice with or without P7 ethanol treatment. In all experimental groups, β-Gal was expressed mainly in the hippocampus with the strongest expression in the granule cell layer of dentate gyrus. In addition, β-Gal was expressed in pyramidal neurons and parvalbumin (PV) neurons in CA1–3 pyramidal layer and in astrocytes scattered around the CA1–3 region although PV neurons were only examined at P30 because of the low PV expression at P8. β-Gal was also expressed in the anteroventral/anteromedial (AV/AM) thalamus and the retrosplenial (Rs) and Tbr1-positive (+) layer 6 cortices. β-Gal-expressing PV neurons were also found in the cortex such as Rs, while β-Gal was barely detected in somatostatin neurons in any brain regions examined. Such region and cell specific β-Gal expression was significantly higher in P8 brains than P30 brains in various brain regions. P7 ethanol reduced β-Gal expression in the CA1–3 pyramidal layer, Tbr1 + cortical layer 6, and the AV/AM thalamus at P8 or P30 or both. Although P7 ethanol decreased PV cells in CA2–3 pyramidal layers as reported, it decreased β-Gal+ PV cells more drastically. The active RA signaling found in PV neurons and the effects of P7 ethanol on the signaling suggest that reduced RA signaling by P7 ethanol may disturb PV cell maturation and enhance long-lasting brain abnormalities.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 797-807"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural remodeling of medium spiny neurons in the tail of the striatum and stress-related behavioral alterations after early handling and adolescent stress in male rats","authors":"Negar Kayedi-Bakhtiari,&nbsp;Jafar Vatanparast","doi":"10.1016/j.ibneur.2026.01.004","DOIUrl":"10.1016/j.ibneur.2026.01.004","url":null,"abstract":"<div><div>The tail of the striatum (TS), the most distal part of the striatum, integrates sensory and value-based information and plays a critical role in threat responses. However, its vulnerability to stress remains underexplored. Here, we examined the effects of early handling (EH), chronic social defeat stress (SD) in late adolescence, and their combination (EH-SD) on anxiety- and depression-like behaviors, as well as dendritic morphology and spine density of TS medium spiny neurons (MSNs) in male rats. SD induced anxiety- and depression-like behaviors in the elevated plus maze and forced swim test, whereas EH conferred resilience against these effects. Structural analysis of Golgi-Cox–stained MSNs revealed that EH and EH-SD increased average dendritic process length without affecting branching or total dendritic length. SD markedly elevated dendritic spine density, while EH reduced it; combined EH-SD prevented the SD-induced increase. Although the changes in the total length of dendritic spines in MSNs did not reach a significant level between groups, there was a trend towards increase in the EH and EH-SD groups and a decrease in the SD group, leading to an estimate of the total number of MSN spines did not differ between groups. It seems that EH promotes structural adaptations linked to circuit stabilization, whereas SD enhances excitatory connectivity of TS MSNs, potentially heightening sensitivity to stress-related sensory inputs. Together, the findings identify the TS as a critical site of structural plasticity in stress and early-life experience, and suggest a link between MSN morphology and resilience or vulnerability to stress-related behavioral outcomes.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 101-111"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tracing the threads: How toxic metals contribute to neurodegeneration","authors":"Elyse Wiebe ,&nbsp;Zaccheaus Olayiwola ,&nbsp;Olamide Adebiyi","doi":"10.1016/j.ibneur.2025.12.008","DOIUrl":"10.1016/j.ibneur.2025.12.008","url":null,"abstract":"<div><div>Brain disorders affect more than one in three people globally, representing a leading cause of disability and morbidity. While the etiology of several of these disorders remains elusive, it is increasingly evident that both genetic and environmental factors contribute to their onset and progression. Given the persistent effects of environmental exposures on biological systems, this review highlights the role of heavy metals (particularly lead, mercury, vanadium, and chromium) in altering behaviour and contributing to the development of neurodegenerative and demyelinating diseases, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. We discuss the sources of human and animal exposure to these metals, focusing on the underlying mechanisms by which they promote neurotoxicity, including oxidative stress, mitochondrial dysfunction, protein aggregation, and disruption of the blood–brain barrier. Additionally, we explore how exposure affects genetic and epigenetic interactions and provide epidemiological data linking metal toxicity to brain disorders. By exploring evidence from animal models and human epidemiological studies, with public health relevance, we extend our discussion beyond descriptive neurotoxicology to highlight exposure to these metals as a unifying upstream driver of various brain disorders. Finally, considering gaps in current knowledge, particularly regarding the impact of transgenerational exposures, we propose directions for future research. These insights not only enhance our understanding of metal-induced neurodegeneration but also underscore the need for targeted public health interventions and policies to reduce exposure, especially in vulnerable populations and communities.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 34-48"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145838510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shared genetic architecture of psychiatric disorders and ocular diseases: Evidence from genome-wide analyses","authors":"Zhao-yang Zhang ,&nbsp;Huan-xi Liu ,&nbsp;Xiao-jia Ma ,&nbsp;Ting-ting Wang ,&nbsp;Xiang-wen Wang ,&nbsp;Wei-jian Han ,&nbsp;Cong Zhou ,&nbsp;Jun-jie Luan ,&nbsp;Ping Sun","doi":"10.1016/j.ibneur.2026.02.003","DOIUrl":"10.1016/j.ibneur.2026.02.003","url":null,"abstract":"<div><h3>Objective</h3><div>Psychiatric disorders are frequently comorbid with ocular diseases, yet the shared genetic basis and potential causal links remain unclear. This study aimed to systematically investigate the shared genetic architecture, bidirectional causality, and implicated biological pathways between common psychiatric disorders and ocular diseases.</div></div><div><h3>Methods</h3><div>We analyzed four psychiatric disorders and eight ocular diseases using an integrative genome-wide analytical framework. We used linkage disequilibrium score regression (LDSC) to estimate genome-wide genetic correlations and local genetic correlation analysis (LAVA) to identify region-specific shared signals. Bidirectional Mendelian randomization (MR) was performed to assess causal relationships. Shared loci were identified using conditional/conjunctive false discovery rate (cond/conjFDR) and evaluated by colocalization. Variants were then annotated and mapped to genes using FUMA, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment and protein–protein interaction (PPI) network analyses to prioritize pathways and hub genes.</div></div><div><h3>Results</h3><div>LDSC revealed significant genetic correlations between anxiety disorder and conjunctivitis, and between major depressive disorder (MDD) and several ocular diseases, including cataract, conjunctivitis, and keratitis. LAVA further confirmed shared, directionally consistent local genetic effects between MDD and these ocular phenotypes across multiple genomic regions. Bidirectional MR suggested that MDD increases the risk of cataract, conjunctivitis, and keratitis, with evidence for bidirectional causality between cataract and MDD. The conjFDR analysis (conjFDR &lt; 0.05) identified approximately 70 independent shared loci (lead SNPs). Functional annotation prioritized representative SNPs with potential functional and regulatory evidence, including rs1029871 and rs678 for bipolar disorder–cataract, rs1042602 for MDD–cataract, and rs12185233 and rs17651549 shared between schizophrenia and both cataract and conjunctivitis. Enrichment analyses of mapped genes suggested that pathways related to hyaluronic acid and amino acid metabolism, cholinergic signaling, and immune–inflammatory processes may contribute to the comorbidity between psychiatric and ocular diseases.</div></div><div><h3>Conclusion</h3><div>This genome-wide study reveals genetic links between psychiatric and ocular diseases and provides evidence for bidirectional causality in selected phenotypes. Metabolism–inflammation–related pathways may contribute to comorbidity along the eye–brain axis, offering leads for future mechanistic validation.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 232-243"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146170474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep deprivation and memory: A neurobiological perspective","authors":"Kehinde O. Adeniji BSc, MSc ,&nbsp;Olumayowa O. Igado DVM, MSc, PhD ,&nbsp;Funmilayo E. Olopade MBBS, MPH, MSc, PhD ,&nbsp;Omowumi M. Femi-Akinlosotu BDS, MSc, PhD","doi":"10.1016/j.ibneur.2026.01.010","DOIUrl":"10.1016/j.ibneur.2026.01.010","url":null,"abstract":"<div><div>Memory consolidation and the preservation of cognitive function are fundamentally influenced by sleep. Lack of sleep affects synaptic plasticity and neurogenesis, as well as oxidative stress and neuroinflammation, all of which impair memory accuracy, cognitive flexibility, and attention. The behavioural repercussions include decreased learning ability, attentional problems, emotional dysregulation, and heightened vulnerability to false memories. This review examines the neurobiological impact of sleep deprivation on memory and cognition, emphasising how the brain systems performing these functions are disrupted by insufficient sleep. The distinct sleep stages that are in support of declarative, procedural, and emotional memory, drawing on contemporary concepts such as the synaptic homeostasis hypothesis and the active system consolidation theory, were emphasised. We highlighted how sleep deprivation can affect important areas, especially the hippocampus, and cause problems with neurotransmitter systems and immune regulation. Preventative and therapeutic approaches, such as pharmacological supports, behavioural interventions, and the cognitive advantages of recovery sleep and naps, were also enumerated. These insights on how sleep and memory interact are vital for enhancing learning outcomes, mental health, and long-term brain resilience.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 170-180"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physical exercise as a non-pharmacological strategy to enhance glymphatic function","authors":"Arman Ghayourvahdat ,&nbsp;Hannaneh Azimizonuzi ,&nbsp;Moslem Ahmed","doi":"10.1016/j.ibneur.2026.01.014","DOIUrl":"10.1016/j.ibneur.2026.01.014","url":null,"abstract":"<div><div>The glymphatic system plays a critical role in clearing metabolic waste and neurotoxic proteins from the brain, and its dysfunction is implicated in neurodegenerative diseases such as Alzheimer’s disease (AD). Emerging evidence indicates that physical exercise enhances glymphatic function through multiple mechanisms, including increased cerebrospinal fluid (CSF) influx, improved perivascular clearance, astrocytic aquaporin-4 (AQP4) polarization, and modulation of vascular and sleep-dependent processes. Preclinical studies demonstrated that voluntary wheel running and aerobic exercise reduce amyloid-β (Aβ) accumulation, attenuate neuroinflammation, and improve cognitive performance in both aging and AD mouse models, with benefits being highly dependent on AQP4 expression and the timing of intervention. Translational evidence in humans showed that structured aerobic and multicomponent exercise increases glymphatic and meningeal lymphatic activity, enhances vascular dynamics, reduces systemic inflammation, and improves sleep quality, leading to measurable cognitive gains. Despite these promising findings, methodological challenges—such as limitations of non-invasive imaging, difficulty establishing causality, and reliance on short-term interventions—highlight the need for longitudinal, multimodal studies that integrate imaging, cardiovascular, sleep, and cognitive metrics. Collectively, these data suggest that exercise represents a potent non-pharmacological strategy to augment glymphatic clearance, preserve neural homeostasis, and reduce the risk of cognitive decline. This review will summarize evidence on exercise-induced glymphatic enhancement, highlight mechanisms, and identify research gaps for future studies on brain health.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 206-217"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146165244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating the impact of intracerebroventricular norepinephrine on spatial memory in rats: Insights into sporadic Alzheimer’s pathogenesis","authors":"Mohammad Amir Sharifi Moien,&nbsp;Seyed Javad Saghravanian,&nbsp;Masoud Fereidoni","doi":"10.1016/j.ibneur.2025.12.012","DOIUrl":"10.1016/j.ibneur.2025.12.012","url":null,"abstract":"<div><div>One consequence of stress is the increased release of norepinephrine (NE) in the central nervous system, primarily driven by activation of the sympathetic nervous system. Given the importance of chronic stress in the development and progression of Alzheimer’s disease (AD), clarifying the specific contributions of stress-related pathways, including the sympathetic axis and the hypothalamic-pituitary-adrenal (HPA) axis, is critical. In this study, we examined the effects of repeated central NE administration, as a potential contributor to stress-related cognitive impairment, on spatial memory in rats, alone or in combination with a low-dose streptozotocin (STZ) model of sporadic AD. Forty-nine rats were assigned to seven groups: control (no treatment), sham (saline; i.c.v.), low-dose streptozotocin (0.5 mg/kg, i.c.v.), norepinephrine administration at either 1 (adolescent) or 3 (adult) months of age (30 or 50 μg, respectively; i.c.v.), and co-administration of norepinephrine with streptozotocin at 1 or 3 months of age. Spatial memory was assessed using the Morris Water Maze test. Norepinephrine administration during adolescence and adulthood impaired spatial memory similar to streptozotocin in different parameters of the MWM, with adult rats showing the most significant vulnerability (p &lt; 0.001). However, co-administration of both substances did not exacerbate the impairment caused by each alone. The results suggest that norepinephrine may impair cognition through mechanisms distinct from those of STZ-induced deficits. Additionally, they raise questions about the contribution of the sympathetic axis of chronic stress to the progression of sporadic AD.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 84-93"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145921807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated serum trimethylamine N-oxide (TMAO) and trimethyllysine in patients with amyotrophic lateral sclerosis (ALS): An exploratory case–control study","authors":"Salvatore Sotgia ,&nbsp;Angelo Zinellu ,&nbsp;Stefano Zoroddu ,&nbsp;Maria Ida Pateri ,&nbsp;Eleonora Loi ,&nbsp;Andrea Pisano ,&nbsp;Angela Sabalic ,&nbsp;Davide Tutedde ,&nbsp;Ana Florencia Vega-Benedetti ,&nbsp;Francesca Floris ,&nbsp;Monica Puligheddu ,&nbsp;Paolo Valera ,&nbsp;Patrizia Zavattari ,&nbsp;Giuseppe Borghero ,&nbsp;Roberto Madeddu","doi":"10.1016/j.ibneur.2026.02.006","DOIUrl":"10.1016/j.ibneur.2026.02.006","url":null,"abstract":"<div><div>Trimethylamine N-oxide (TMAO) is a gut microbiota–derived metabolite implicated in protein homeostasis, inflammation, and chronic disease, but its relevance in amyotrophic lateral sclerosis (ALS) remains poorly characterized. In this exploratory pilot study, we quantified circulating TMAO and related trimethylammonium-containing compounds in a Sardinian ALS cohort using targeted LC–MS/MS. Serum samples were collected under fasting conditions from 12 ALS patients and 8 age- and sex-matched healthy controls. Median serum TMAO levels were markedly higher in ALS patients than in controls (27.9 vs. 4.0 µmol/L, P &lt; 0.05), with substantial inter-individual variability in the ALS group (range 2.4–125.0 µmol/L). Trimethyllysine (TML) concentrations were also significantly elevated in ALS (0.43 vs. 0.34 µmol/L, P &lt; 0.05), whereas choline, carnitine, betaine, ergothioneine, and γ-butyrobetaine levels did not differ between groups. Most ALS patients were receiving acetyl-<span>L</span>-carnitine (ALCAR) supplementation, suggesting that ALCAR intake may contribute to the observed metabolite profiles. Overall, these findings indicate alterations in trimethylammonium-containing compound metabolism in ALS and underscore the need for larger, well-controlled studies to determine whether such changes reflect disease-related mechanisms, treatment effects, or their interaction.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 227-231"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146170475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-time autonomic responses to insulin-induced hypoglycaemia in volunteers with type I diabetes compared to controls","authors":"Maria Bitsch Poulsen ,&nbsp;Christina Brock ,&nbsp;Peter Oketa-Onyut Julu","doi":"10.1016/j.ibneur.2025.12.014","DOIUrl":"10.1016/j.ibneur.2025.12.014","url":null,"abstract":"<div><h3>Objective</h3><div>Hypoglycaemia is a severe risk of insulin-treatment in diabetes, and in type 1 diabetes (T1D), the normal counterregulatory autonomic mechanisms are diminished. This study investigated the recovery of both parasympathetic and sympathetic tone from hypoglycaemia to normoglycemia in T1D in comparison to controls.</div></div><div><h3>Methods</h3><div>Six individuals with T1D without complications and six age and sex-matched controls were included in this explorative acute intervention study. Electrocardiogram, skin blood flow (SBF, sympathetic measure), cardiac vagal tone (CVT, parasympathetic measure), and plasma glucose were measured at baseline, at hypoglycaemia, and at 30-, 60-, 120-, and 240-minutes post-hypoglycaemia.</div></div><div><h3>Results</h3><div>Insulin injection induced hypoglycaemia with a reduction of CVT in both controls and individuals with T1D, but no consistent response in SBF. Normoglycemia was reached by 120-minutes, though T1D showed delayed glucose recovery at 30- and 60-minutes with an overshoot at 240-minutes. SBF showed no consistent changes but was lower in T1D at 240-minutes. CVT increased consistently, recovering after 60-minutes in the individuals with T1D and 30-minutes in the controls, with a heightened at 240-minutes in the individuals with T1D.</div></div><div><h3>Conclusion</h3><div>CVT as a measure of cardiac parasympathetic function responds consistently to both hypoglycaemia and during recovery in individuals with T1D and controls, but SBF as a measure of cutaneous sympathetic function does not. There are defective counterregulatory mechanisms in T1D shown by delayed recovery of blood glucose and rebound overactivity of both cardiac parasympathetic tone and sympathetic cutaneous vasoconstriction.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 119-124"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling seizure interruptions: Excitability dynamics in spike-wave activity","authors":"Gilles van Luijtelaar PhD ,&nbsp;Bob de Ruijter MSc","doi":"10.1016/j.ibneur.2026.05.005","DOIUrl":"10.1016/j.ibneur.2026.05.005","url":null,"abstract":"<div><div>Neuronal activity during a spike–wave complex (SWC) consists of highly synchronized firing of neuronal populations followed by a period of neuronal silence. It may manifest as an interictal spike or repetitive. Cortical excitability during the ascending and descending slope of the spike and during the three wave components of Spike-Wave discharges is examined in a well-established genetic rodent model of absence epilepsy using single-pulse electrical stimulation. The probability of interrupting ongoing SWDs and the electrical evoked response were assessed. Single-pulse stimulation could interrupt SWDs, primarily in the first second of an SWD, but also later, irrespective of whether stimulation occurred during the spike or wave. The amplitude of the P1 recorded from the somatosensory cortex was significantly higher during the descending phase of the spike than during the spike’s ascending phase and the wave components. During the wave component, P1 amplitudes increased toward the end. The P1 made during non-REM sleep resembled those of the wave. The differences between the first second and later might be due to differences in coupling between cortex and thalamus and to the dynamics of the intraspike frequency, the differences between the two phases of the spike to the readiness and possibility to fire, while the inhibition during the wave is due to hyperpolarization. Further, the possibility of interrupting an SWD by a single pulse is not related to the changes in cortical excitability, but seems caused by an interruption of the oscillatory cortico-thalamo-cortical network driving SWDs.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 808-819"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}