BMC NeurosciencePub Date : 2025-01-28DOI: 10.1186/s12868-025-00926-y
Julian E Alecu, Veronika Sigutova, Razvan-Marius Brazdis, Sandra Lörentz, Marios Evangelos Bogiongko, Anara Nursaitova, Martin Regensburger, Laurent Roybon, Kerstin M Galler, Wolfgang Wrasidlo, Beate Winner, Iryna Prots
{"title":"NPT100-18A rescues mitochondrial oxidative stress and neuronal degeneration in human iPSC-based Parkinson's model.","authors":"Julian E Alecu, Veronika Sigutova, Razvan-Marius Brazdis, Sandra Lörentz, Marios Evangelos Bogiongko, Anara Nursaitova, Martin Regensburger, Laurent Roybon, Kerstin M Galler, Wolfgang Wrasidlo, Beate Winner, Iryna Prots","doi":"10.1186/s12868-025-00926-y","DOIUrl":"10.1186/s12868-025-00926-y","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease (PD) is a neurodegenerative disorder characterized by protein aggregates mostly consisting of misfolded alpha-synuclein (αSyn). Progressive degeneration of midbrain dopaminergic neurons (mDANs) and nigrostriatal projections results in severe motor symptoms. While the preferential loss of mDANs has not been fully understood yet, the cell type-specific vulnerability has been linked to a unique intracellular milieu, influenced by dopamine metabolism, high demand for mitochondrial activity, and increased level of oxidative stress (OS). These factors have been shown to adversely impact αSyn aggregation. Reciprocally, αSyn aggregates, in particular oligomers, can impair mitochondrial functions and exacerbate OS. Recent drug-discovery studies have identified a series of small molecules, including NPT100-18A, which reduce αSyn oligomerization by preventing misfolding and dimerization. NPT100-18A and structurally similar compounds (such as NPT200-11/UCB0599, currently being assessed in clinical studies) point towards a promising new approach for disease-modification.</p><p><strong>Methods: </strong>Induced pluripotent stem cell (iPSC)-derived mDANs from PD patients with a monoallelic SNCA locus duplication and unaffected controls were treated with NPT100-18A. αSyn aggregation was evaluated biochemically and reactive oxygen species (ROS) levels were assessed in living mDANs using fluorescent dyes. Adenosine triphosphate (ATP) levels were measured using a luminescence-based assay, and neuronal cell death was evaluated by immunocytochemistry.</p><p><strong>Results: </strong>Compared to controls, patient-derived mDANs exhibited higher cytoplasmic and mitochondrial ROS probe levels, reduced ATP-related signals, and increased activation of caspase-3, reflecting early neuronal cell death. NPT100-18A-treatment rescued cleaved caspase-3 levels to control levels and, importantly, attenuated mitochondrial oxidative stress probe levels in a compartment-specific manner and, at higher concentrations, increased ATP signals.</p><p><strong>Conclusions: </strong>Our findings demonstrate that NPT100-18A limits neuronal degeneration in a human in vitro model of PD. In addition, we provide first mechanistic insights into how a compartment-specific antioxidant effect in mitochondria might contribute to the neuroprotective effects of NPT100-18A.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"8"},"PeriodicalIF":2.4,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143057953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of subclinical hypothyroidism during pregnancy on mtDNA methylation in the brain of rat offspring.","authors":"Liangzhuo Xie, Yangling Huang, Xiande Ma, Xiaoqiu Ma, Jian Wang, Tianshu Gao, Wei Chen","doi":"10.1186/s12868-025-00930-2","DOIUrl":"10.1186/s12868-025-00930-2","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to investigate the impact of subclinical hypothyroidism (SCH) during pregnancy on mitochondrial DNA (mtDNA) methylation in the brain tissues of rat offspring.</p><p><strong>Materials and methods: </strong>Sixteen SD rats were randomly divided into two groups: control group (CON) and SCH group. BS-seq sequencing was used to analyze mtDNA methylation levels in the offspring's brain tissues; the 2,7-dichlorofluorescin diacetate (DCFH-DA) probe method was employed to detect reactive oxygen species (ROS) levels in brain tissues; electron microscopy was utilized to observe the mitochondrial structure in the hippocampal tissues of the offspring.</p><p><strong>Results: </strong>In the analysis of differentially methylated regions (DMRs), the mitochondrial chromosome in the SCH group exhibited 23 DMRs compared to the control group. ROS levels in the brain tissues of the SCH group were significantly higher than those in the control group (P < 0.05). The mitochondrial structure in the hippocampus of the SCH group was less intact compared to the CON group.</p><p><strong>Conclusion: </strong>Subclinical hypothyroidism in pregnant rats may alter the mtDNA methylation pattern in the brains of their offspring, potentially affecting mitochondrial function and structure.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"6"},"PeriodicalIF":2.4,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11762456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143036866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Association between apolipoprotein E ε4 status and the risk of Alzheimer's disease: a meta-analysis.","authors":"Zijun Ren, Zhenting Guan, Qingliang Guan, Hongjian Guan, Hongjian Guan","doi":"10.1186/s12868-024-00914-8","DOIUrl":"10.1186/s12868-024-00914-8","url":null,"abstract":"<p><strong>Background: </strong>The apolipoprotein E ε4 (APOE ε4) status has a controversial role in predicting Alzheimer's disease (AD) factors. This meta-analysis assessed AD event risk in patients with APOE ε4 status.</p><p><strong>Materials and methods: </strong>The relevant English-language articles were identified by searching the Cochrane Library, EMBASE, and PubMed databases. The prognostic significance of APOE ε4 status in AD patients was examined on the basis of pooled hazard ratios (HRs).</p><p><strong>Results: </strong>A total of 22 studies published after 1987, including 571,800 patients, were included. Consequently, APOE ε4 status was a risk factor for disease-free survival (DFS, HR = 2.033; 95% confidence interval [CI] = 1.589-2.602; P = 0.000; I 2 = 93.1%) in patients with AD. Additionally, subgroup analysis suggested that the ROC curve was the main risk factor among patients with AD.</p><p><strong>Conclusions: </strong>AD patients with different events are managed via different methods; however, the present meta-analysis suggests an increased risk of AD events in patients with different APOE ε4 statuses.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"5"},"PeriodicalIF":2.4,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11761182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143036864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BMC NeurosciencePub Date : 2025-01-24DOI: 10.1186/s12868-024-00917-5
Abdullah Bin Dawood
{"title":"Age predicts peak gamma frequency and N1 amplitude of visual evoked potential.","authors":"Abdullah Bin Dawood","doi":"10.1186/s12868-024-00917-5","DOIUrl":"10.1186/s12868-024-00917-5","url":null,"abstract":"<p><p>The current study investigated whether the age of healthy adults could predict the peak gamma frequency and the peak amplitudes of VEP components (N1, P2). 49 healthy participants (aged between 19 and 52 years) underwent EEG recordings during a visual task eliciting clear gamma frequency oscillations and VEP activities. After eliminating noisy and outlier data, data from 41 participants were analysed using simple linear regression. The results indicated that age was a significant predictor of peak gamma frequency and the peak amplitude of VEP-N1 but not the peak amplitude of VEP-P2. Age was negatively associated with peak gamma frequency and the peak amplitude of VEP-N1. These findings support previous research indicating that ageing is associated with decreased cortical inhibition, highlighting the importance of GABA in maintaining cortical E-I balance.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"7"},"PeriodicalIF":2.4,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143036858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BMC NeurosciencePub Date : 2025-01-22DOI: 10.1186/s12868-025-00927-x
Utkarsha A Singh, Soumya Iyengar
{"title":"Delta opioid receptors affect acoustic features of song during vocal learning in zebra finches.","authors":"Utkarsha A Singh, Soumya Iyengar","doi":"10.1186/s12868-025-00927-x","DOIUrl":"10.1186/s12868-025-00927-x","url":null,"abstract":"<p><p>Delta-opioid receptors (δ-ORs) are known to be involved in associative learning and modulating motivational states. We wanted to study if they were also involved in naturally-occurring reinforcement learning behaviors such as vocal learning, using the zebra finch model system. Zebra finches learn to vocalize early in development and song learning in males is affected by factors such as the social environment and internal reward, both of which are modulated by endogenous opioids. Pairs of juvenile male siblings (35-day-old) were systemically administered a δ-OR-selective antagonist naltrindole or vehicle (controls) for a period of 10 days. The acoustic structure of songs differed across treated and control groups at adulthood (120 days). Naltrindole-treated birds had a significantly lower pitch, mean frequency, and frequency modulation than controls, whereas there was no difference in the number of songs in naltrindole-treated and control siblings. Since the opioid and dopaminergic systems interact, we decided to study whether blocking δ-ORs during the sensitive period led to changes in dopaminoceptive neurons in Area X, a song control nucleus in the basal ganglia. Interestingly, compared with controls, naltrindole-treated birds had higher numbers of DARPP-32-positive medium spiny neurons and potentially excitatory synapses in Area X. We show that manipulating δ-OR signaling during the learning phase resulted in alterations in the acoustic features of song and had long term effects on dopaminergic targets within the basal ganglia in adulthood. Our results suggest that endogenous opioids regulate the development of cognitive processes and the underlying neural circuitry during the sensitive period for learning.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"4"},"PeriodicalIF":2.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143021827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Identification of key genes associated with oxidative stress in ischemic stroke via bioinformatics integrated analysis.","authors":"Gaiyan Li, Yu Cheng, Shanshan Ding, Qianyun Zheng, Lanqiong Kuang, Ying Zhang, Ying Zhou","doi":"10.1186/s12868-024-00921-9","DOIUrl":"10.1186/s12868-024-00921-9","url":null,"abstract":"<p><strong>Background: </strong>Ischemic stroke (IS) is a common cerebrovascular disease. Although the formation of atherosclerosis, which is closely related to oxidative stress (OS), is associated with stroke-related deaths. However, the role of OS in IS is unknown.</p><p><strong>Methods: </strong>OS-related key genes were obtianed by overlapping the differentially expressed genes (DEGs) between IS and normal control (NC) specimens, IS-related genes, and OS-related genes. Then, we investigated the mechanism of action of key genes. Subsequently, protein-protein interaction (PPI) network and machine learning algorithms were utilized to excavate feature genes. In addition, the network between feature genes and microRNAs (miRNAs) was established to investigate the regulatory mechanism of feature genes. Finally, quantitative PCR (qPCR) was utilized to validate the expression of feature genes with blood specimens.</p><p><strong>Results: </strong>A total of 42 key genes related to OS were acquired. Enrichment analysis indicated that the key genes were associated with oxidative stress, reactive oxygen species, lipid and atherosclerosis, and cell migration-related pathways. Then, 6 feature genes (HSPA8, NCF2, FOS, KLF4, THBS1, and HSPA1A) related to OS were identified for IS. Besides, 6 feature genes and 255 miRNAs were utilized to establish a feature genes-miRNA network which contained 261 nodes and 277 edges. At last, qPCR results revealed that there was a trend for higher expression of FOS, KLF4, and HSPA1A in IS specimens than in NC specimens. Additionally, HSPA8 expression was significantly decreased in the IS specimens, which was consistent with the findings of the GEO database analysis.</p><p><strong>Conclusion: </strong>In conclusion, 6 feature genes (HSPA8, NCF2, FOS, KLF4, THBS1, and HSPA1A) related to OS were mined by bioinformatics analysis, which might provide a new insights into the evaluation and treatment of IS.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"3"},"PeriodicalIF":2.4,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11727628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142977154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BMC NeurosciencePub Date : 2025-01-08DOI: 10.1186/s12868-024-00923-7
Zhanhua Lu, Kun Huang
{"title":"Protective effect of silencing lncRNA HCP5 against brain injury after intracerebral hemorrhage by targeting miR-195-5p.","authors":"Zhanhua Lu, Kun Huang","doi":"10.1186/s12868-024-00923-7","DOIUrl":"10.1186/s12868-024-00923-7","url":null,"abstract":"<p><strong>Background: </strong>Intracerebral hemorrhage (ICH) is a common subtype of stroke, characterized by a high mortality rate and a tendency to cause neurological damage. This study aims to investigate the role and mechanisms of lncRNA HCP5 in ICH.</p><p><strong>Methods: </strong>We simulated ICH in vivo by injecting collagenase into rats and established an in vitro model using hemoglobin-treated BV2 cells. HCP5 and miR-195-5p levels were quantified by RT-qPCR. mNSS score was used to evaluate neurological deficits in the rats. The dry-wet weight method assessed the degree of brain edema. Cell viability and apoptosis rates were determined using the CCK-8 assay and flow cytometry, respectively. The targeting relationship between HCP5 and miR-195-5p was confirmed using dual-luciferase reporter assays and RNA immunoprecipitation. ELISA was utilized to measure inflammatory factors, and commercial kits were used to detect MDA and ROS levels.</p><p><strong>Results: </strong>In the ICH model rats, HCP5 levels were significantly elevated. It was also found that silencing HCP5 significantly alleviated brain edema and neurological deficits in the ICH rats, and there was a marked improvement in ICH-induced neuroinflammation and oxidative stress. Moreover, HCP5 was found to sponge miR-195-5p, and inhibiting miR-195-5p could counteract the neuroprotective effects of silencing HCP5. Similar results were obtained in the in vitro experiments with BV2 cells.</p><p><strong>Conclusions: </strong>Silencing HCP5 can alleviate brain edema, neurological dysfunction, neuroinflammation, and oxidative stress caused by ICH via miR-195-5p.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"2"},"PeriodicalIF":2.4,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11708098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BMC NeurosciencePub Date : 2025-01-03DOI: 10.1186/s12868-024-00920-w
Su-Min Park, Yong-Hun Oh, Ga-Hyun Lim, Ju-Hyun An, Jin-Hwan Lee, Byoung-Joo Gwag, So-Jung Won, Kyoung-Won Seo, Hwa-Young Youn
{"title":"Crisdesalazine alleviates inflammation in an experimental autoimmune encephalomyelitis multiple sclerosis mouse model by regulating the immune system.","authors":"Su-Min Park, Yong-Hun Oh, Ga-Hyun Lim, Ju-Hyun An, Jin-Hwan Lee, Byoung-Joo Gwag, So-Jung Won, Kyoung-Won Seo, Hwa-Young Youn","doi":"10.1186/s12868-024-00920-w","DOIUrl":"10.1186/s12868-024-00920-w","url":null,"abstract":"<p><p>Microglia/macrophages participate in the development of and recovery from experimental autoimmune encephalomyelitis (EAE), and the macrophage M1 (pro-inflammatory)/M2 (anti-inflammatory) phase transition is involved in EAE disease progression. We evaluated the efficacy of crisdesalazine (a novel microsomal prostaglandin E2 synthase-1 inhibitor) in an EAE model, including its immune-regulating potency in lipopolysaccharide-stimulated macrophages, and its neuroprotective effects in a macrophage-neuronal co-culture system. Crisdesalazine significantly alleviated clinical symptoms, inhibited inflammatory cell infiltration and demyelination in the spinal cord, and altered the phase of microglial/macrophage and regulatory T cells. Crisdesalazine promoted the M1 to M2 phase transition in macrophages (immunomodulation) and reduced neuronal necrosis (neuroprotection) in vitro. This is the first study to directly demonstrate the therapeutic effects of a microsomal prostaglandin E2 synthase-1 inhibitor in an EAE model and its ability to alter macrophage polarization, suggesting that it may be a new therapeutic option for the treatment of patients affected by multiple sclerosis and other autoimmune diseases.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"1"},"PeriodicalIF":2.4,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BMC NeurosciencePub Date : 2024-12-31DOI: 10.1186/s12868-024-00913-9
Ross Mandeville, Hooman Sedghamiz, Perry Mansfield, Geoffrey Sheean, Chris Studer, Derrick Cordice, Ghodsieh Ghanbari, Atul Malhotra, Shamim Nemati, Jejo Koola
{"title":"Deep learning enhanced transmembranous electromyography in the diagnosis of sleep apnea.","authors":"Ross Mandeville, Hooman Sedghamiz, Perry Mansfield, Geoffrey Sheean, Chris Studer, Derrick Cordice, Ghodsieh Ghanbari, Atul Malhotra, Shamim Nemati, Jejo Koola","doi":"10.1186/s12868-024-00913-9","DOIUrl":"10.1186/s12868-024-00913-9","url":null,"abstract":"<p><p>Obstructive sleep apnea (OSA) is widespread, under-recognized, and under-treated, impacting the health and quality of life for millions. The current gold standard for sleep apnea testing is based on the in-lab sleep study, which is costly, cumbersome, not readily available and represents a well-known roadblock to managing this huge societal burden. Assessment of neuromuscular function involved in the upper airway using electromyography (EMG) has shown potential to characterize and diagnose sleep apnea, while the development of transmembranous electromyography (tmEMG), a painless surface probe, has made this opportunity practical and highly feasible. However, experience and ability to interpret electrical signals from the upper airway are scarce, and much of the pertinent information within the signal is likely difficult to detect visually. To overcome this issue, we explored the use of transformers, a deep learning (DL) model architecture with attention mechanisms, to model tmEMG data and distinguish between electromyographic signals from a cohort of control, neurogenic, and sleep apnea patients. Our approach involved three strategies to train a generalizable model on a relatively small dataset including, (1) transfer learning using an audio spectral transformer (AST), (2) the use of 6,000 simulated EMG recordings, converted to spectrograms and using standard backpropagation for fine-tuning, and (3) application of regularization to prevent overfitting and enhance generalizability. This DL approach was tested using 177 transoral EMG recordings from a prior study's database that included six healthy controls, five moderate to severe OSA patients, and five amyotrophic lateral sclerosis (ALS) patients with evidence of bulbar involvement (neurogenic injury). Sensitivity and specificity for classifying neurogenic cases from controls were 98% and 73%, respectively, while classifying OSA from controls were 88% and 64%, respectively. Notably, by averaging the predicted probabilities of each segment for individual patients, the model correctly classified up to 82% of control and OSA patients. These results not only suggest a potential to diagnose OSA patients accurately, but also to identify OSA endotypes that involve neuromuscular pathology, which has major implications for clinical management, patient outcomes, and research.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"25 1","pages":"80"},"PeriodicalIF":2.4,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11686987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BMC NeurosciencePub Date : 2024-12-27DOI: 10.1186/s12868-024-00919-3
Andrew Savoy, Katherine L Anderson, Joseph V Gogola
{"title":"The songbird connectome (OSCINE-NET.ORG): structure-function organization beyond the canonical vocal control network.","authors":"Andrew Savoy, Katherine L Anderson, Joseph V Gogola","doi":"10.1186/s12868-024-00919-3","DOIUrl":"10.1186/s12868-024-00919-3","url":null,"abstract":"<p><strong>Background: </strong>Understanding the neural basis of behavior requires insight into how different brain systems coordinate with each other. Existing connectomes for various species have highlighted brain systems essential to various aspects of behavior, yet their application to complex learned behaviors remains limited. Research on vocal learning in songbirds has extensively focused on the vocal control network, though recent work implicates a variety of circuits in contributing to important aspects of vocal behavior. Thus, a more comprehensive understanding of brain-wide connectivity is essential to further assess the totality of circuitry underlying this complex learned behavior.</p><p><strong>Results: </strong>We present the Oscine Structural Connectome for Investigating NEural NETwork ORGanization (OSCINE-NET.ORG), the first interactive mesoscale connectome for any vocal learner. This comprehensive digital map includes all known connectivity data, covering major brain superstructures and functional networks. Our analysis reveals that the songbird brain exhibits small-world properties, with highly connected communities functionally designated as motor, visual, associative, vocal, social, and auditory. Moreover, there is a small set of significant connections across these communities, including from social and auditory sub-communities to vocal sub-communities, which highlight ethologically relevant facets of vocal learning and production. Notably, the vocal community contains the majority of the canonical vocal control network, as well as a variety of other nodes that are highly interconnected with it, meriting further evaluation for their inclusion in this network. A subset of nodes forms a \"rich broker club,\" highly connected across the brain and forming a small circuit amongst themselves, indicating they may play a key role in information transfer broadly. Collectively, their bidirectional connectivity with multiple communities indicates they may act as liaisons across multiple functional circuits for a variety of complex behaviors.</p><p><strong>Conclusions: </strong>OSCINE-NET.ORG offers unprecedented access to detailed songbird connectivity data, promoting insight into the neural circuits underlying complex behaviors. This data emphasizes the importance of brain-wide integration in vocal learning, facilitating a potential reevaluation of the canonical vocal control network. Furthermore, we computationally identify a small, previously unidentified circuit-one which may play an impactful role in brain-wide coordination of multiple complex behaviors.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"25 1","pages":"79"},"PeriodicalIF":2.4,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142891836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}