Brain communications最新文献

{"title":"Celebrating the founding editor of <i>Brain Communications</i>: Tara Spires-Jones.","authors":"David Belin","doi":"10.1093/braincomms/fcag139","DOIUrl":"https://doi.org/10.1093/braincomms/fcag139","url":null,"abstract":"<p><p>Our incoming editor-in-chief pays tribute to the founding editor of <i>Brain Communications</i>, Professor Tara Spires-Jones.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 3","pages":"fcag139"},"PeriodicalIF":4.5,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: The use of 7T MRI in multiple sclerosis: review and consensus statement from the North American Imaging in Multiple Sclerosis Cooperative.","authors":"","doi":"10.1093/braincomms/fcag155","DOIUrl":"https://doi.org/10.1093/braincomms/fcag155","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/braincomms/fcae359.].</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 2","pages":"fcag155"},"PeriodicalIF":4.5,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147824635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GABA_A binding correlates with high-frequency EEG: a possible proxy for depolarization in traumatic brain injury.","authors":"Sudhin A Shah, Ludvik Alkhoury, Isabelle Martin, Ana Radanovic, Giacomo Scanavini, Seyed Hani Hojjati, Gloria C Chiang, Tracy A Butler, Yeona Kang, Keith W Jamison, Amy Kuceyeski, Nicholas D Schiff","doi":"10.1093/braincomms/fcag145","DOIUrl":"https://doi.org/10.1093/braincomms/fcag145","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) frequently results in long-term cognitive and functional deficits, yet routine diagnostic tools often fail to capture the diffuse network dysfunction and underlying neurochemical changes that contribute to poor recovery. Resting-state EEG is sensitive to injury-related abnormalities in neural oscillations, while [¹¹C]flumazenil PET quantifies gamma-aminobutyric acid (GABA_A) receptor availability-a key determinant of inhibitory tone and cortical synchronization-but these modalities are rarely integrated. Linking EEG spectral features to molecular measures of GABA_A function may provide translational biomarkers that bridge non-invasive neurophysiological findings with underlying neurochemical status. The primary aim of this study was to determine whether resting-state EEG spectral features, particularly in the high-frequency beta and gamma bands, track longitudinal changes in GABA_A receptor availability measured with [¹¹C]flumazenil PET in individuals recovering from TBI. A secondary aim was to characterize the persistence of low-frequency abnormalities (increased delta, reduced alpha) over the first year of recovery and explore their potential relevance as non-invasive markers of network dysfunction. We analysed EEG data from 68 subjects with TBI and 75 non-brain-injured controls; longitudinal follow-up EEG data were available for 37 TBI participants and 20 non-brain-injured controls. We found that the TBI subjects exhibited significantly higher delta power and lower alpha power; this remained at the chronic visit. Among the longitudinally studied subjects, a subset of seven TBI participants and six non-brain-injured controls were studied with [¹¹C]flumazenil PET data. We found strong positive correlations between longitudinal changes in [¹¹C]flumazenil PET measured GABA_A receptor availability and concurrent changes in EEG high beta (<i>r</i> ² = 0.79, <i>P</i> < 0.01) as well as low and high gamma power (<i>r</i> ² = 0.71, <i>P</i> < 0.05; <i>r</i> ² = 0.77, <i>P</i> < 0.01) in TBI subjects for the 'eyes-open' condition. These exploratory findings provide preliminary evidence that GABA_A receptor availability, measured via [¹¹C] flumazenil PET, is associated with high-frequency EEG power in TBI. This PET-EEG coupling may reflect underlying changes in excitatory-inhibitory network balance consistent with restoration of fronto-striatal arousal and neuronal membrane 'tone' under the mesocircuit model, although the small sample size of the cohort with multimodal measurements warrants cautious interpretation and further replication. Nonetheless, the observations in this cohort are consistent with a key role of increasing inhibitory activity across fronto-striatal neurons and networks in recovery from TBI.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 3","pages":"fcag145"},"PeriodicalIF":4.5,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: A passive and objective measure of recognition memory in mild cognitive impairment using Fastball memory assessment.","authors":"","doi":"10.1093/braincomms/fcag147","DOIUrl":"https://doi.org/10.1093/braincomms/fcag147","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/braincomms/fcaf279.].</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 2","pages":"fcag147"},"PeriodicalIF":4.5,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13107314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147792090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Convergent structural brain alterations in chronic pain: a multi-metric individual participant data meta-analysis.","authors":"Ryan W J Loke, Oscar Ortiz, Sylvia M Gustin, Michèle Hubli, Clas Linnman, Abigail Livny, Yann Quidé, Paulina S Scheuren, John L K Kramer","doi":"10.1093/braincomms/fcag146","DOIUrl":"https://doi.org/10.1093/braincomms/fcag146","url":null,"abstract":"<p><p>Chronic pain is a leading contributor to all-cause morbidity and disability, encompassing numerous biopsychosocial dimensions that persistently engage complex networks of brain regions. Meta-analyses have advanced our understanding of structural brain differences in chronic pain but rely exclusively on summary statistics which may introduce heterogeneity related to completeness of reporting and differences in methodological approaches. To address these limitations, we conducted the first individual participant data (IPD) meta-analysis of brain structure alterations in chronic pain. Using traditional morphometric measures (i.e. volume, cortical thickness, and surface area) and differential-geometric shape metrics (i.e. intrinsic and extrinsic curvature), we aimed to reveal alterations in brain structure convergent across chronic pain conditions. We hypothesized that chronic pain would be associated with region-specific grey matter reductions in regions previously implicated in chronic pain (e.g. parahippocampal gyrus and insula) and explored whether curvature metrics would reveal additional structural changes. Anatomical MRI images from eight publicly available datasets spanning five conditions and 401 individuals with chronic pain (and 245 age- and sex- matched healthy controls) were analysed: (i) knee osteoarthritis, (ii) chronic low back pain, (iii) fibromyalgia, (iv) migraine, and (v) primary trigeminal neuralgia. FreeSurfer was used to parcellate T1-weighted anatomical images, and metrics for cortical and subcortical regions were extracted. Meta-analysis revealed a range of structural changes in the brain associated with chronic pain. Cortical thinning and volume loss were small and localized to the temporo-occipital regions, including bilateral volumetric reductions in the entorhinal cortex in individuals with chronic pain. Increases in intrinsic curvature were widespread, involving 49 out of 68 cortical regions. No significant alterations were detected in subcortical volumes. Intrinsic curvature and subcortical volumetric estimates had higher levels of inter-study heterogeneity compared to other metrics, reflecting potential condition and sample-specific variability. Leveraging harmonized processing across a large sample size, our novel IPD meta-analysis highlights both widespread and region-specific structural remodelling of chronic pain-related neuroanatomy.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 3","pages":"fcag146"},"PeriodicalIF":4.5,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiscale connectivity framework for working memory network in paediatric acute lymphoblastic leukaemia survivors.","authors":"Rajikha Raja, John O Glass, Ruitian Song, Lisa M Jacola, Tushar Patni, Yimei Li, Wilburn E Reddick","doi":"10.1093/braincomms/fcag137","DOIUrl":"https://doi.org/10.1093/braincomms/fcag137","url":null,"abstract":"<p><p>Working memory impairments are a common late effect in survivors of childhood acute lymphoblastic leukaemia, yet the structural network substrates of these difficulties remain poorly defined. Existing connectomic studies often rely on whole-brain parcellations, overlooking working memory-associated circuitry and multiscale organization. We developed a multiscale structural connectivity framework to investigate working memory-associated networks using diffusion MRI and performed a cross-sectional study with 70 acute lymphoblastic leukaemia survivors and 70 age and sex matched healthy controls. Working memory-relevant regions were identified based on functional activation patterns, and structural connectomes were constructed at two spatial scales: a fine-scale 76-node network and a coarser 24-node network derived from spatially contiguous, architecturally and functionally coherent regional groupings, as defined in the multimodal parcellation atlas of Human Connectome Project. Graph theoretical metrics, clustering coefficient, Eigenvector centrality, local assortativity and participation coefficient were computed to assess local network topology. Group comparisons were conducted with false discovery rate correction for multiple comparisons. Compared to healthy controls, survivors exhibited marked topological shifts. Specifically, clustering and assortativity were increased in the caudate, putamen and thalamus but decreased in the frontoparietal cortex. In contrast, centrality and participation showed the opposite pattern, signalling subcortical segregation and cortical hyperintegration. These effects were consistent across both spatial scales. Additional findings included scale-specific effects unique to the fine scale, as well as heterogeneous fine-scale patterns that resolved into consistent regional changes at the coarse scale. All effects remained significant after false discovery rate correction, highlighting the robustness of the network reorganization. Our framework combining a targeted working memory network with multiscale connectomic analysis proves its worth by revealing structural changes of working memory circuitry in survivors compared to healthy controls. The results show a broad reorganization, with weakened cortical networks and strengthened subcortical circuits, possibly as a form of compensation. These insights sharpen our understanding of treatment-related structural network alterations and point to new targets for future studies of cognitive outcomes and rehabilitation.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 2","pages":"fcag137"},"PeriodicalIF":4.5,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147824659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurophysiological, imaging and neurobiological markers of central fatigue in multiple sclerosis.","authors":"Alberto Benelli, Elisa Tatti, Rosa Cortese, Elisa Massucco, Ludovico Luchetti, Marco Battaglini, Javier Cudeiro, Anna de Mauro, Jian Zhang, Domenico Plantone, Patrizio Pasqualetti, Delia Righi, Francesco Neri, Maria Laura Stromillo, Alessandra Cinti, Alessandro Giannotta, Francesco Lomi, Adriano Scoccia, Giuseppe Lai, Nicola De Stefano, Monica Ulivelli, Simone Rossi","doi":"10.1093/braincomms/fcag134","DOIUrl":"https://doi.org/10.1093/braincomms/fcag134","url":null,"abstract":"<p><p>Central fatigue affects 80% of patients with multiple sclerosis, with 60% of them claiming it as the most disabling symptom. Current research often independently explores neurophysiological, structural, or functional imaging and biological underpinnings of fatigue, thus lacking a multidimensional perspective. Here, we used a multidimensional approach to investigate the functional, structural and biological underpinnings of fatigue in MS and to assess the relative contribution of each factor. A cross-sectional study was conducted with 41 patients with relapsing-remitting multiple sclerosis and 21 healthy controls (female 14) (HC). MS patients were recruited by including only those with an Expanded Disability Status Scale score < 4, and were categorized as fatigued (MS-F: 19, Female 13, FSS ≥ 4) or non-fatigued (MS-NF: 22, Female 11, FSS < 4). Over five phases, participants underwent Transcranial Magnetic Stimulation, resting-state Electroencephalography, structural and functional Magnetic Resonance, clinical assessments, and blood tests for neurofilament light chain, serum glial fibrillary acidic protein and cytokine levels. Data were analysed using both non-parametric and parametric tests, based on the data distribution. Finally, a decision-tree model was applied to predict patient group assignment. Neurophysiologically, the two patient groups differed in several domains. Those with fatigue had increased θ-band EEG power in frontocentral regions with eyes open. Transcranial Magnetic Stimulation findings indicated significantly lower intracortical facilitation in the MS-F group. Neuroimaging revealed stronger functional connectivity between nodes of the Default Mode Network, between the left temporal node and the right prefrontal node, in the MS-F group. Furthermore, fractional anisotropy via Diffusion Tensor Imaging showed reduced white matter integrity in the corticospinal tracts and corpus callosum in these patients. No significant differences were observed in lesion load, brain volumes, clinical/psychological measures, or blood sample findings linked with neurodegeneration or inflammation; the only psychological variable that differed between the two groups was the depression scale score, with MS-F patients reporting higher scores than MS-NF patients. The decision tree analysis identified both ICF and significantly lower fractional anisotropy values as the most accurate predictors of fatigue, with a classification accuracy of 84.2%. Results highlight the importance of a multidisciplinary approach in defining central fatigue in multiple sclerosis, which would emerge through subtle, subclinical, regional abnormalities of myelin integrity and clearly manifest neurophysiological evidence of impaired glutamatergic activity in motor areas. They also suggest possible biomarkers for the diagnosis of fatigue, possibly useful for eventual targeting novel neuromodulatory treatments.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 3","pages":"fcag134"},"PeriodicalIF":4.5,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gonadotropin-releasing hormone alleviates chronic pain-related depression in male mice by rebalancing the anterior cingulate cortex excitatory-inhibitory processes via the protein kinase C/Erb-B2 receptor tyrosine kinase 4 pathway.","authors":"Yanmei Huang, Yunfeng Chen, Xueqin Liu, Yang Xu, Ling Chen, Wenyu Cao, Xiaolin Zhong","doi":"10.1093/braincomms/fcag138","DOIUrl":"https://doi.org/10.1093/braincomms/fcag138","url":null,"abstract":"<p><p>Depression is a common comorbidity of chronic pain. Gonadotropin-releasing hormone (GnRH) and its receptor (GnRHR) expressed in the central nervous system are involved in non-reproductive functions. Herein, we aimed to elucidate the role and mechanism of action of GnRH in pain-related depression like behaviour in a mouse model. And we found that both GnRH and GnRHR were down-regulated in the anterior cingulate cortex of mice that were subjected to chronic pain-induced depression with complete Freund's adjuvant. Specifically, either systemic treatment with GnRH agonists or GnRH overexpression in the anterior cingulate cortex effectively ameliorated the chronic pain-induced depression-like behaviour via GnRHR signalling. Moreover, GnRHR co-localized with both excitatory and inhibitory neurons, and GnRH agonists or overexpressed GnRH rescued the complete Freund's adjuvant-stimulated imbalance of excitatory-inhibitory neurons in the anterior cingulate cortex. Chemogenetic activation of anterior cingulate cortex neurons reversed GnRH agonist-induced improvement in depression-like behaviour in complete Freund's adjuvant-treated mice. Furthermore, this specific role of GnRH was dependent on the activation of protein kinase C and Erb-B2 receptor tyrosine kinase 4 signalling pathway. Therefore, our findings indicate that GnRH/GnRHR is involved in the development of chronic pain-related depression, which may through rebalancing the excitatory-inhibitory neurons via the activation of protein kinase C/Erb-B2 receptor tyrosine kinase 4 pathway. Thus, GnRH could be a potential target for the treatment of chronic pain-related depression.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 2","pages":"fcag138"},"PeriodicalIF":4.5,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147824712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"White matter hyperintensities, retinal vascular calibre and changes in age-related hearing loss.","authors":"David P Q Clark, Cammie Tran, Sultana Monira Hussain, Catherine Robb, Carlene Britt, Robyn L Woods, Paul A Yates, Amy Brodtmann, Mohamed Salah Khlif, Geoffrey Donnan, Gary Rance, John J McNeil","doi":"10.1093/braincomms/fcag133","DOIUrl":"https://doi.org/10.1093/braincomms/fcag133","url":null,"abstract":"<p><p>Cerebral small vessel disease may contribute to age-related hearing loss pathogenesis by reducing blood flow to the cochlea and/or areas of the brain important for hearing. Cerebral white matter hyperintensities (WMHs) and retinal vascular calibre are both considered to be non-invasive markers of cerebral small vessel health. This study investigated the relationship between age-related hearing loss, retinal vascular calibre and WMHs in older adults using data from the ASPirin in Reducing Events in the Elderly (ASPREE) trial, including participants who underwent hearing assessment, retinal photography and brain magnetic resonance imaging. Participants were free of evident cardiovascular disease at recruitment between 2010 and 2014. Retinal vascular calibre was measured using central retinal arteriolar and venular equivalents. Total brain WMH volumes were calculated using an automated lesion prediction algorithm and further segmented as deep WMH and periventricular WMH. Hearing acuity was assessed using pure tone audiometry and speech perception in background noise. A total of 308 participants (aged 70+) were included. In both cross-sectional and longitudinal analyses no associations were found between baseline central retinal arteriolar equivalent, central retinal venular equivalent, total WMH, deep WMH or periventricular WMH in relation to changes in audiometric 0.5, 4 and 8 kHz thresholds or speech perception after adjusting for confounding factors. This study identified no relationship between retinal vascular calibre, WMH volumes and hearing function in healthy older adults. This suggests that microvascular changes in the eye and brain may occur independently of changes in auditory function in older individuals.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 2","pages":"fcag133"},"PeriodicalIF":4.5,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147824644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal interhemispheric neuromodulation sharpens synaptic and neurobehavioral inhibition in stroke.","authors":"João Castelhano, Felix Duecker, Ana Carolina Xavier, Nádia Canário, Isabel C Duarte, Sónia Afonso, Ana Gabriel Marques, Cecilia Lourenço, Filipe Carvalho, Jorge Lains, Angela Neves, João Sargento Freitas, Gustavo Cordeiro Santo, Antero J Abrunhosa, Alexander T Sack, Miguel Castelo-Branco","doi":"10.1093/braincomms/fcag119","DOIUrl":"https://doi.org/10.1093/braincomms/fcag119","url":null,"abstract":"<p><p>Hemispheric functional asymmetries are a key aspect of human brain organization. Revealing how causal manipulations of hemispheric (im)balances dynamically change pre- and post-synaptic GABA regulation, in terms of mean and variance changes, is essential to understand the plasticity of brain asymmetries in health and disease. This has direct implications for treatment approaches in stroke relying on interhemispheric inhibition using transcranial magnetic stimulation. We investigated neurobehavioral and neurochemical effects of cortical stimulation using a unique multimodal brain imaging and stimulation set-up, in both healthy and unilaterally lesioned hemispheres, in stroke. We performed two molecular imaging sessions measuring GABA receptor levels, with sham and real neurostimulation, functional magnetic resonance imaging (MRI) and GABA neurospectroscopy, all in the same day. We found that noninvasive inhibitory neuromodulation of interhemispheric interactions causes pre- and post-synaptic sharpening of GABA neurotransmitter and receptor levels, providing a mechanism of action for transcranial magnetic stimulation contralateral inhibitory protocols in stroke. Moreover, we found a positive association between GABA neurotransmitter and receptor levels, suggesting increased synaptic coupling. This discovered plasticity mechanism, based on correlated reduction of pre- and post-synaptic variability, represents a basic principle underlying long-range inhibitory hemispheric interactions and allows for the stabilization of synapses and rebalancing of brain activity in disorders of hemispheric imbalance, such as stroke.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"8 2","pages":"fcag119"},"PeriodicalIF":4.5,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}