BMC Neuroscience最新文献

{"title":"Distinct neural circuits processing pleasant and unpleasant sounds: an fMRI-based approach.","authors":"Faten Mana Aldhafeeri","doi":"10.1186/s12868-025-00975-3","DOIUrl":"https://doi.org/10.1186/s12868-025-00975-3","url":null,"abstract":"<p><strong>Background: </strong>Investigating how the human brain processes the emotional valance of sounds is critical for understanding sensory, emotional, and motor integration at the neurobiological level. The current study utilized functional magnetic resonance imaging (fMRI) to investigate the differential brain activation patterns elicited by pleasant, unpleasant, and neutral sounds from the International Affective Digital Sounds (IADS-2) collection. Thirty healthy volunteers listened to these sounds under fMRI, followed by post-scan ratings of valence (pleasant versus unpleasant) and arousal (calm versus exciting).</p><p><strong>Results: </strong>Average ratings did not differ from IADS-2 norms. Pleasant sounds significantly activated brain regions implicated in reward and positive affect, including the mPFC, ventral anterior cingulate cortex, and inferior frontal gyrus, compared to neutral sounds. Alternatively, unpleasant sounds elicited stronger and more widespread activation, particularly in the amygdala, nucleus accumbens, insula, and cerebellum, regions associated with negative affect and aversive learning.</p><p><strong>Conclusion: </strong>These results demonstrate the pivotal contributions of the amygdala in identifying unpleasant stimuli and of the mPFC in assessing pleasant auditory inputs, expand our current understanding of affective regulation at the neural circuit level, and provide a foundation for the development of sound-based interventions to treat auditory-emotional disorders such as misophonia and anxiety.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"52"},"PeriodicalIF":2.3,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941891","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":"Hybrid molecule SA-10 and its PLGA nanosuspension protect human and rodent retinal ganglion cells against neuronal injury.","authors":"Jennifer H Pham, Wei Zhang, Kim-Tuyen T Le, Bindu Kodati, Charles E Amankwa, Biddut DebNath, Gretchen A Johnson, Thien T Bui, Rachel Y Gitter, Jonah P Gutierrez, Brendon R Hatfield, Rojan Satyal, Ella R Sinnott, Raghu R Krishnamoorthy, Suchismita Acharya, Dorota L Stankowska","doi":"10.1186/s12868-025-00971-7","DOIUrl":"https://doi.org/10.1186/s12868-025-00971-7","url":null,"abstract":"<p><strong>Background: </strong>Glaucoma is a leading cause of blindness characterized by retinal ganglion cell (RGC) degeneration. SA-10, a dual-acting compound with ROS scavenging and NO-donating properties, was evaluated to enhance RGC survival and function in models of oxidative stress, ischemia/reperfusion (I/R) injury, and neurotrophic factor (NF) deprivation.</p><p><strong>Methods: </strong>SA-10-loaded nanoparticles (SA-10-NP) with a size of 279.6 ± 20.9 nm, polydispersity index of 0.34, and encapsulation efficiency of 80.6% were synthesized and tested for sustained release over 28 days. I/R injury was induced by elevating intraocular pressure to 120 mmHg for 60 min in C57BL/6J mice, followed by SA-10-NP treatment (1% w/v). Retinal ganglion cell function and survival were evaluated using PERG and PVEP. Oxidative stress in primary RGCs and retinal explants was induced using endothelin-3 (ET-3), and the effects of SA-10 (10 µM) on ROS levels were assessed. In ex vivo human retinal explants (HREs), SA-10 treatment effects on oxidative stress markers NRF2 and HMOX1 were analyzed.</p><p><strong>Results: </strong>SA-10-NP improved PERG amplitudes (112.96% in females, p < 0.01) and PVEP amplitudes (67.53% in females, p < 0.01), preserving RGC density in both central and mid-peripheral regions. Immunohistochemistry showed upregulation of Hmox1 and downregulation of TNF-α in the SA-10-NP-treated group. SA-10 significantly reduced ROS levels in primary RGCs and retinal explants exposed to endothelin-3 (ET-3), decreasing fluorescence intensity by 25.9% (p < 0.01) and 14.7% (p < 0.0001), respectively. SA-10 upregulated oxidative stress markers (NRF2 and HMOX1) and enhanced RGC survival in NF-deprived HREs.</p><p><strong>Conclusions: </strong>SA-10 demonstrated significant ROS reduction and preserved RGC survival and function in both I/R mouse models and HREs, with immunohistochemistry confirming upregulation of Hmox1 and downregulation of TNF-α in the SA-10-NP-treated group. SA-10-NP provided sustained drug delivery and bioavailability, showcasing strong neuroprotective effects and offering a potential therapeutic strategy for glaucomatous optic neuropathy and other neurodegenerative conditions.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"51"},"PeriodicalIF":2.3,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941946","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":"Visual change-related brain potentials elicited by changes in doll hair color in school-aged children.","authors":"Mizuki Kozaki, Ryo Mizuno, Masaya Suzuki, Yasuyuki Koike, Natsuko Doi, Koji Inui","doi":"10.1186/s12868-025-00970-8","DOIUrl":"10.1186/s12868-025-00970-8","url":null,"abstract":"<p><p>Change-related brain responses are specifically elicited when the regularity of a continuous sensory stimulus is disrupted and are recorded by electroencephalography or magnetoencephalography. These responses are one of the higher brain functions representing memory-based comparison processes between the current and previous sensory states. The present study aimed to record change-related visual evoked potentials in children aged 6-10 years. Pictures of a doll were presented for 1.5 s, and participants were given the task of quickly pressing a button when glasses appeared on the doll, which occurred in 5% of trials. In the remaining 95% of trials, one third used pictures with no change, while the others used a similar picture but with a hair color change, from rose to yellow or from brown to pink, 1000 ms after the stimulus onset. The results obtained showed that in all 37 children tested, the abrupt change in hair color elicited clear biphasic responses consisting of occipital positivity at approximately 130 ms (P130) followed by negativity at 250 ms. The P130 latency decreased linearly up to 92 months of age and remained stable thereafter, suggesting that this method may serve as an objective tool for assessing brain development in children. In addition, it could potentially be used to evaluate whether and how specific toys influence neural processing at different developmental stages.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"50"},"PeriodicalIF":2.3,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12337465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820511","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 subanesthetic dose of ketamine on motor and cognitive outcomes of harmaline-induced essential tremor model: a focus on Lingo-1 and inflammatory pathways.","authors":"Mehran Ilaghi, Zeynab Pirmoradi, Zahra Esmaili, Shamim Hosseinalipour, Leili Rouhi, Adel Soltanizadeh, Mohsen Nakhaie, Kiana Sharififar, Moazamehosadat Razavinasab, Mohammad Shabani","doi":"10.1186/s12868-025-00966-4","DOIUrl":"10.1186/s12868-025-00966-4","url":null,"abstract":"<p><strong>Introduction: </strong>Essential tremor (ET) is a common neurodegenerative disorder characterized by action tremors and various non-motor symptoms. This study investigated the potential therapeutic effects of ketamine, an NMDA receptor antagonist with known GABA modulatory and anti-inflammatory properties, in a harmaline-induced model of ET in mice. We also evaluated the changes in expression of inflammatory interleukin 6 (IL-6) as well as Leucine rich repeat and Immunoglobin-like domain-containing protein 1 (Lingo-1), a prominent gene involved in the pathogenesis of ET.</p><p><strong>Methods: </strong>Male Swiss Webster mice were divided into four groups: control, harmaline (10 mg/kg), ketamine (8 mg/kg), and harmaline + ketamine. Tremor severity, muscle strength, locomotor activity, anxiety-like behavior, and passive avoidance learning were assessed. Cerebellar expression of Lingo-1 and IL-6 was analyzed using real-time PCR.</p><p><strong>Results: </strong>Ketamine did not significantly reduce harmaline-induced tremors but improved muscle strength deficits in the wire grip test. In the open field test, ketamine normalized some harmaline-induced changes in locomotor activity and grooming behavior. No significant differences were observed in passive avoidance learning across groups. At the molecular level, ketamine did not mitigate the harmaline-induced increase in IL-6 expression, and Lingo-1 expression was not significantly altered by either harmaline or ketamine treatment.</p><p><strong>Conclusion: </strong>Our findings suggest that ketamine has limited efficacy in the harmaline ET model, showing some improvements in motor function and anxiety-like behavior but failing to address core tremor symptoms or modulate inflammatory and Lingo-1 pathways. These results highlight the complex nature of ET pathophysiology and the need for further research into targeted therapeutic approaches.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"49"},"PeriodicalIF":2.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12317601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764474","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":"Valproate-vitamin E co-treatment preserved cortico-callosal white matter integrities in cypermethrin co-exposed pentylene tetrazole induced seizure.","authors":"Aminu Imam, Oluwadamilola Eunice Ajibola, Aalimah Akinosho Akorede, Omamuyovwi Meashack Ijomone, Moyosore Salihu Ajao","doi":"10.1186/s12868-025-00967-3","DOIUrl":"10.1186/s12868-025-00967-3","url":null,"abstract":"<p><strong>Background: </strong>Epilepsy is characterized by recurrent seizures and neurological consequences, which may be associated with impaired myelin and glial integrity, and exacerbated by environmental neurotoxicants. Environmental neurotoxicants, such as Cypermethrin (CPM), may heighten these impairments, worsening seizure outcomes. This study investigates the effects of Cypermethrin (CPM) on Pentylenetetrazole (PTZ)-induced seizures and the Vitamin E (Vit E) and valproate (VAP) co-interventions on myelin and glial integrity.</p><p><strong>Methods: </strong>Histochemical and immunohistochemical analyses for hematoxylin and eosin (H&E), myelin basic protein (MBP), ionized calcium-binding adaptor molecule 1 (IBA1), glial fibrillary acidic protein (GFAP), and oligodendrocyte transcription factor 2 (OLIG-2) were conducted on cerebral white matter and corpus callosum tissues. The density of stained cells and immunoreactivity obtained with ImageJ was subjected to one-way analysis of variance.</p><p><strong>Results: </strong>Immunohistochemistry revealed that cypermethrin exposure in PTZ-induced seizure rats led to marked neuronal, oligodendroglial, and myelin loss, accompanied by substantial glial activation in both cerebral white matter and corpus callosum. Interventional ingestions of VAP and Vit E, especially when combined, substantially reduced both microglial activation and reactive astrogliosis, thereby consequently preventing oligodendrocyte and neuronal loss, thus preserving both cerebral white matter and callosal myelin.</p><p><strong>Conclusions: </strong>These findings highlight the potential of pyrethroid insecticides to exacerbate the neurological consequences of epilepsy, specifically causing myelin damage via glial activation. Also, the putative therapeutic synergy of antioxidant supplementation in epilepsy and neurotoxicity management was obvious.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"48"},"PeriodicalIF":2.3,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12312494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752283","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":"Structural changes of tubulin by interacting with Δ⁹-tetrahydrocannabinol: in-vitro and theoretical studies.","authors":"Mina Mohammadkhani, Mostafa Jarah, Dariush Gholami, Gholamhossein Riazi, Hadi Rezazadeh","doi":"10.1186/s12868-025-00957-5","DOIUrl":"10.1186/s12868-025-00957-5","url":null,"abstract":"<p><strong>Background: </strong>There is growing evidence of the contribution of microtubule dynamics to dendritic spine changes, synaptic plasticity, axonal transportation, and cell polarity. Besides, one of the well-studied effects of Cannabis on human behavior is memory disability. As Δ⁹-tetrahydrocannabinol (Δ⁹-THC) is the most pivotal chemical of Cannabis, we investigated the effect of Δ⁹-THC on microtubule dynamicity and the structural study of tubulin (microtubule monomer).</p><p><strong>Results: </strong>Our results show that Δ⁹-THC changes microtubule dynamicity compared to the control group. The turbidity assay results demonstrated that Δ⁹-THC reduces microtubule polymerization in a concentration-dependent manner. Circular Dichroism spectroscopy also studied the structural changes of the purified tubulin, which revealed significant changes in the secondary structure of the tubulin. Furthermore, Silico studies predicted one binding site for Δ⁹-THC on β-tubulin.</p><p><strong>Conclusions: </strong>We concluded that Δ⁹-THC could reduce the microtubule's stability, which may conversely affect brain function by microtubule dynamic changes caused by secondary structural changes of tubulin and preventing tubulin-tubulin interaction.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"47"},"PeriodicalIF":2.3,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12312531/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752282","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 repetitive mechanical tactile stimulation interventions with stationary and moving patterns on paired-pulse depression.","authors":"Hiraku Watanabe, Sho Kojima, Naofumi Otsuru, Hideaki Onishi","doi":"10.1186/s12868-025-00960-w","DOIUrl":"10.1186/s12868-025-00960-w","url":null,"abstract":"<p><strong>Background: </strong>Repetitive somatosensory stimulation (RSS) reduces paired-pulse depression (PPD), reflecting GABAergic inhibition in the primary somatosensory cortex (S1). This effect may vary by tactile stimulation pattern. Therefore, this study aimed to clarify the effects of RSS intervention with stationary and moving pattern tactile stimulation on PPD.</p><p><strong>Results: </strong>In a crossover study of 15 healthy males, RSS with a stationary pattern showed a non-significant trend toward increased PPD (corrected p = 0.088), while the moving pattern showed no effect. A strong negative correlation was found between baseline PPD and its change rate (r = - 0.837, p < 0.001), indicating that greater baseline S1 inhibition predicted a larger reduction after RSS.</p><p><strong>Conclusion: </strong>RSS effects on GABAergic inhibition in S1 depend on the tactile stimulation pattern, emphasizing the importance of tactile stimulus design in modulating somatosensory cortex activity.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"46"},"PeriodicalIF":2.3,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717362","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":"Mir-199a-3p aggravates neuroinflammation in an Alzheimer's disease transgenic mouse model by promoting M1-polarization microgliaMir-199a-3p M1.","authors":"Chenyang Wang, Xiaolu Bu, Mengyao Cao, Yunyu Lian, Haocong Ling, Mo You, Junfei Yi, Xiaoya Gao, Duobin Wu, Yang Li","doi":"10.1186/s12868-025-00965-5","DOIUrl":"10.1186/s12868-025-00965-5","url":null,"abstract":"<p><strong>Background: </strong>Chronic neuroinflammation, driven by M1-polarized microglia, is a core pathological mechanism of Alzheimer's disease (AD). Elevated expression levels of miR-199a-3p and pro-inflammatory cytokines were detected in the hippocampi of AD transgenic mice and in LPS-stimulated BV2 microglial cells. We hypothesized that miR-199a-3p exacerbates neuroinflammation by promoting M1 microglial polarization in AD progression. M1 （AD） 。 AD LPS BV2 miR-199a-3p 。 miR-199a-3p AD M1 。 OBJECTIVE: To explore the role of miR-199a-3p in AD-associated neuroinflammation. miR-199a-3p AD 。 METHODS: AD transgenic (APPswe/PSEN1dE9) mice and LPS-treated BV2 cells were used to assess miR-199a-3p effects in vivo and in vitro. Inflammatory cytokines and markers for microglial cell typing were detected. Transcriptome sequencing was performed on miR-199a-3p-modulated BV2 cells, and the sequencing data were cross-analyzed with public databases to predict miR-199a-3p-mediated pathways.AD （APPswe/PSEN1dE9） LPS BV2 miR-199a-3p 。。 miR-199a-3p BV2 ，， miR-199a-3p 。 RESULTS: Intracerebroventricular administration of miR-199a-3p agomir exacerbated amyloid deposition and impaired cognitive function in AD mice, and promoted microglial polarization toward the M1 phenotype. Conversely, treatment with miR-199a-3p antagomir attenuated AD pathology and suppressed M1 polarization. In LPS treated BV2 cells, miR-199a-3p mimics promoted M1 polarization, while inhibitors reversed this effect. Transcriptome analysis revealed that miR-199a-3p downregulated WDR76, subsequently suppressing cell cycle-associated pathways, IL-17 signaling, and FOXO pathways, resulting in an increase in the proportion of M1 type microglia. miR-199a-3p agomir AD ， M1 。， miR-199a-3p AD M1 。 LPS BV2 ，miR-199a-3p M1 ，。，miR-199a-3p WDR76，、 IL-17 FOXO ， M1 。 CONCLUSION: MiR-199a-3p aggravates neuroinflammation of AD by promoting M1-polarization microglia. These findings highlight miR-199a-3p as a potential therapeutic target for AD.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"45"},"PeriodicalIF":2.3,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12288326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706266","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":"Anatomical and behavioral characterization of three hemiplegic animal models.","authors":"Mei Liu, Lingling Xu, Gefei Cheng, Yang Yang, Likun Yang, Yuhai Wang","doi":"10.1186/s12868-025-00961-9","DOIUrl":"10.1186/s12868-025-00961-9","url":null,"abstract":"<p><strong>Background: </strong>Hemiplegia is characterized by muscle weakness on one side of the body, often resulting from damage to the brain, spinal cord, or associated nerves. This condition commonly occurs due to strokes, traumatic brain injuries (TBI), or spinal cord injuries (SCI), which can damage corticospinal neurons (CSNs) and the corticospinal tract (CST). However, there is still a notable lack of comprehensive studies that systematically characterize the anatomical and behavioral aspects of these hemiplegic animal models.</p><p><strong>Objective: </strong>This study aimed to validate and compare existing models of TBI, stroke, and SCI in order to identify the most suitable preclinical hemiplegia models for future research.</p><p><strong>Method: </strong>Using viral-based retrograde tracing, we first mapped the cortical distribution of CSNs responsible for hindlimb movement. Anterograde and retrograde viral tracing techniques were then employed to label and evaluate the damage to CSNs and the CST in three models: photothrombotic stroke, Feeney's weight-drop TBI, and T10 hemi-section SCI. We also conducted behavioral tests to assess spontaneous motor function recovery, including open field and rotarod tests for gross motor function, as well as beam walking and irregular ladder walking tasks for assessing skilled motor function.</p><p><strong>Results: </strong>Our findings revealed that the CSNs controlling hindlimb movement are concentrated in the hindlimb region of the primary somatosensory cortex (S1HL). In the TBI and stroke models, there was complete destruction of ipsilateral CSNs in the S1HL and loss of CST fibers governing hindlimb movement. In the SCI model, ipsilateral CST fibers below T10 were also lost. After 8 weeks post-injury, all three groups of hemiplegic mice showed improvements in motor function, with gross motor function returning to normal levels; however, the recovery of skilled motor function was only modest. Notably, the degree of improvement in fine motor skills varied among the hemiplegia models, with mice subjected to brain injury (stroke and TBI) demonstrating significantly greater recovery in fine motor skills compared to those with SCI.</p><p><strong>Conclusion: </strong>We confirmed and validated previous hemiplegia models by damaging CSNs or CST controlling hindlimb movement. Post-injury, gross motor function gradually returned to normal levels across all groups, whereas recovery of skilled motor function was limited. Furthermore, there were significant differences in the recovery of skilled motor function between brain injury models and the SCI model. These hemiplegic mouse models are valuable tools for studying post-injury skilled motor functions.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"44"},"PeriodicalIF":2.3,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12278650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144681964","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":"Post-stroke butyrate treatment shows sex-dependent microglial responses but does not improve outcomes in a mouse model of endothelin-1 sensory motor stroke.","authors":"Ashley de Witte, Juliana Montoya Sanchez, Emerson Daniele, Jingan Chen, Yibang Fan, Pranav Khatri, Daniela Lozano Casasbuenas, Angel Zhang, Kathryn G Todd, Maryam Faiz, Matthew Churchward","doi":"10.1186/s12868-025-00959-3","DOIUrl":"10.1186/s12868-025-00959-3","url":null,"abstract":"<p><strong>Background: </strong>Stroke induces gut dysbiosis and reduces microbial production of short-chain carboxylic acids (SCCAs), which negatively correlates with stroke outcomes. Previous studies have demonstrated that SCCA supplementation can improve functional recovery, with one recent study suggesting this occurs via modulation of microglial responses. However, the effects of individual SCCAs on microglial responses remain unclear, particularly across sexes and following a more clinically relevant, post-stroke treatment protocol. To address this gap, we investigated the effect of post-stroke supplementation with butyrate on stroke outcomes and microglial responses in both male and female mice over time.</p><p><strong>Results: </strong>Post-stroke butyrate treatment produced sex-specific microglial responses. In females, butyrate increased microglial ramification at chronic timepoints in vivo and enhanced IL6 release following IFNγ stimulation in vitro. These microglial changes were not observed in males. Despite the distinct microglial responses, butyrate treatment did not correlate with improved stroke outcomes in either sex, as measured by lesion volume and functional recovery.</p><p><strong>Conclusions: </strong>Our findings reveal previously unknown sex differences in microglial responses to butyrate following stroke. Despite these microglial changes in females, butyrate treatment did not improve functional outcomes in either sex, suggesting that sex-specific optimization of dosing and delivery may be needed for therapeutic efficacy.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"43"},"PeriodicalIF":2.4,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658348","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}