Journal of Neuroscience Research最新文献

{"title":"Characterizing Non-Traumatic Spinal Cord Injury in Neonatal Sprague Dawley Rats","authors":"Reggie M. Ridlen,&nbsp;Mathew Burke,&nbsp;Caitlin Wesley,&nbsp;Huyen Tran Le,&nbsp;Luke Farrell,&nbsp;Kristine McGrath,&nbsp;Catherine A. Gorrie","doi":"10.1002/jnr.70086","DOIUrl":"10.1002/jnr.70086","url":null,"abstract":"<div>\u0000 \u0000 <p>Spinal cord injuries (SCI) can occur from either traumatic or non-traumatic causes. While traumatic spinal cord injury (TSCI), caused by acute external forces, is well-researched, non-traumatic spinal cord injury (NTSCI), arising from chronic conditions like tumors and infections, is often underreported and misclassified. NTSCI is increasingly recognized as a major cause of SCI globally, particularly affecting the elderly and infants. Despite its prevalence, research on NTSCI remains limited, necessitating new models to understand its pathophysiology. This study introduces a novel, repeatable model for NTSCI in both neonatal (9 days post-partum) and adult rats (9 weeks post-partum), simulating chronic compression injuries. The model uses 3D-printed (PLA) spacers to induce mild–moderate compression in the lower thoracic vertebrae. Six weeks of spinal cord compression resulted in locomotor deficits and cellular changes consistent with hypoxic–ischemic injury due to disrupted blood flow, without significant long-term inflammation or astrogliosis. This versatile model can be easily adapted for different age groups, for graded injury severities, and for different injury durations. It offers a promising avenue for understanding and treating chronic compression NTSCI, addressing a critical gap in current research. This model can be used in future research to test and understand the effectiveness and pathophysiology of decompression and cellular interventions in response to chronic compression NTSCI.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 11","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145431726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolution of Axonal Injury in the Closed Head Impact Model of Engineered Rotational Acceleration in Adult Ferrets","authors":"Justin L. Krieg,&nbsp;Kosta Antolis,&nbsp;Carl Hooper,&nbsp;Hasini Kapuwelle,&nbsp;Rebecca George,&nbsp;William T. O'Brien,&nbsp;Stuart J. McDonald,&nbsp;Anna V. Leonard,&nbsp;Renée J. Turner,&nbsp;Frances Corrigan","doi":"10.1002/jnr.70090","DOIUrl":"https://doi.org/10.1002/jnr.70090","url":null,"abstract":"<div>\u0000 \u0000 <p>Concussion-related symptoms, such as impaired balance, slower processing speed, attention deficits, memory dysfunction, and irritability, are thought to result from diffuse axonal injury (DAI), characterized by selective damage to white matter axons. Axons subjected to this mechanical stretch injury exhibit diverse pathological changes, including disruption of axonal transport, neurofilament compaction and degradation, myelin sheath disruption, and loss of sodium channels required for action potential generation and propagation. These distinct forms of axonal pathology may evolve differentially over time and preferentially localize to specific white matter tracts. In this study, we employed the clinically relevant ferret model of concussion using the closed head impact model of engineered rotational acceleration (CHIMERA). 55 male ferrets were randomly allocated to sham or injury groups and then to either 24 h, 72 h, or 14d survival time points. We confirmed that axonal transport disruption and neurofilament pathology represent independent processes, with minimal colocalization but a shared peak of around 72 h following injury. Furthermore, we observed a persistent loss of ankyrin-G, a critical anchoring protein for sodium channels at the node of Ranvier, up to 14d postinjury, suggesting that the resultant impairment in axonal transmission may underlie many concussion symptoms. Indeed, injured ferrets displayed significant deficits in balance, working memory, spatial memory, and recognition memory. These findings demonstrate that the CHIMERA model in ferrets recapitulates key axonal pathologies and their associated clinical manifestations following concussion. This model offers a valuable platform for investigating the temporal evolution of axonal injury and developing targeted therapeutic interventions to mitigate concussion-related deficits.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 11","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145385101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Slc20a2 Deficiency Increases Susceptibility to CNS Demyelination Possibly Through Th17 Cells","authors":"Yueni Zhang,&nbsp;Xin Wang,&nbsp;Yaqiong Ren,&nbsp;Zitong Zhang,&nbsp;Ying Li,&nbsp;Ziyue Peng,&nbsp;Chao Xu,&nbsp;Liang Cheng,&nbsp;Xue Zhang","doi":"10.1002/jnr.70088","DOIUrl":"https://doi.org/10.1002/jnr.70088","url":null,"abstract":"<div>\u0000 \u0000 <p>Primary familial brain calcification (PFBC) is a rare inherited neurodegenerative disorder characterized by abnormal brain calcium-phosphate (Ca-Pi) deposits along microvessels or inside neuronal cells. Eight genes have been linked to PFBC, with the <i>SLC20A2</i> being the earliest identified. <i>SLC20A2</i> encodes PiT-2, which is crucial for Pi homeostasis in the cerebrospinal fluid (CSF). In <i>Slc20a2</i> homozygous knockout (HO) mice, the neurotoxic effects resulting from pathological CSF-Pi accumulation and the unique brain transcriptome suggested that the absence of PiT-2 might lead to myelin abnormalities. However, the myelin morphology and content under <i>Slc20a2</i> deficiency remained largely unknown, and these were quantitatively investigated in this study. The results indicated no direct demyelination in the brains of <i>Slc20a2</i>-HO mice, but an increased susceptibility to demyelination under the induction of oligodendrocyte-toxic cuprizone (CPZ). The enhanced susceptibility was related to a greater infiltration of Th17 cells in the brain parenchyma, accompanying an exacerbation of brain calcification in <i>Slc20a2</i> deficiency.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 11","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145385146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Newborn Auditory Brainstem Response and Sudden Infant Death Syndrome","authors":"Sarah E. Maylott,&nbsp;Guangyu Zeng,&nbsp;Tiffany S. Leung,&nbsp;Catalina Sanchez Montenegro,&nbsp;Alexia Barrios,&nbsp;Arushi Malik,&nbsp;Rafael E. Delgado,&nbsp;Christine F. Delgado,&nbsp;Elizabeth A. Simpson","doi":"10.1002/jnr.70083","DOIUrl":"https://doi.org/10.1002/jnr.70083","url":null,"abstract":"<div>\u0000 \u0000 <p>Sudden infant death syndrome (SIDS)—the sudden and unexplained death of a seemingly healthy infant, &lt; 1 year old—may be associated with abnormalities in the brain regions that underlie breathing and arousal during sleep. While post-mortem studies suggest abnormalities in SIDS infants' brainstems, there are no studies of these infants' brainstem function before death. One way to assess the function of the brainstem is with auditory brainstem response (ABR), a routine hearing-screening method that noninvasively measures the brainstem's response to sound. We hypothesized that anomalies in newborns' ABR measures may predict SIDS. We integrated two secondary datasets and examined ABRs of newborns who later died of SIDS (<i>n</i> = 11) compared to a normative sample (<i>n</i> = 198,990), using existing archived records of neonatal ABR results from a sample of newborns born in Florida. As hypothesized, infants who died from SIDS were more likely than non-SIDS infants to have abnormal ABRs as newborns. Children who died of SIDS appeared to have shorter latencies to the trough that follows peak V in the left ear than children without SIDS. However, our expert-rated data failed to replicate this finding, suggesting it is unlikely to reflect a true effect. Understanding the association between SIDS and ABR may facilitate more accurate identification of an infant's risk for SIDS at birth, enabling increased monitoring, which may facilitate interventions and improve survivorship.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 11","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145385102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Moderate Chronic Treadmill Exercise Slows Dopaminergic Neuron Loss in a Rat Model of Parkinson's Disease and Alters RNA Content of Circulating Plasma Exosomes","authors":"Bruce A. Citron,&nbsp;Maynard Guzman,&nbsp;Bobak Shapdoor,&nbsp;Pranela Rameshwar,&nbsp;Arpine Sokratian,&nbsp;Amaan L. Shaikh,&nbsp;Anya E. Mausoof,&nbsp;Andrew B. West,&nbsp;Vedad Delic","doi":"10.1002/jnr.70084","DOIUrl":"10.1002/jnr.70084","url":null,"abstract":"<p>Exercise has been reported to improve outcomes in patients with Parkinson's disease, but the exact biological mechanisms remain incompletely understood. This study was conducted to determine whether chronic moderate treadmill exercise prevents dopaminergic neuron loss and Lewy body-like inclusion burden in a preclinical model of PD. This study also sought to identify plasma exosome bound “exerkines” with potential to induce neuroprotective brain adaptations. Benefits of exercise are thought to be achieved in part through nucleic acids, lipids, and peptides termed exerkines abundant during exercise. These exerkines can induce cell-specific exercise adaptations culminating in neuroprotection. Membrane-free exerkines are subject to degradation in blood and may not effectively cross the blood-brain barrier to induce brain adaptations to exercise, limiting their inter-organ signaling potential. This led us to hypothesize that exerkines, bioactive RNAs in particular, may be selectively packaged into exosomes and released into plasma during exercise. Exosomes are small extracellular vesicles, selectively packaged and released by cells, with likely important differences in composition at rest, during injury and disease, and in response to exercise. Exosomes have been demonstrated to play a major role in inter-organ communication. Chronic exercise was found to provide neuroprotection to dopaminergic neurons in the substantia nigra pars compacta, without affecting Lewy body-like inclusion burden in the nigra or the striatum. Plasma exosomal RNA was isolated from age-matched exercising and sedentary non-PD rats and sequenced. We report 27 unique RNAs upregulated in the exosomes of exercisers, 3 mRNAs with clear neuroprotective potential.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12516300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145280489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Cell RNA-Seq and Machine Learning Reveal Key Feature Genes of Astrocyte in Perioperative Neurocognitive Disorders","authors":"Le Zhao,&nbsp;Zhumei Chen,&nbsp;Xuelian Ma,&nbsp;Xinjin Chi","doi":"10.1002/jnr.70085","DOIUrl":"https://doi.org/10.1002/jnr.70085","url":null,"abstract":"<div>\u0000 \u0000 <p>Perioperative neurocognitive disorder (PND) is common in older patients after anesthesia and surgery, significantly increasing morbidity and mortality. However, the role of astrocytes in its pathogenesis remains limitedly understood. Here, we analyzed 9976 and 9484 single-cell transcriptomes from hippocampal cells of aged mice undergoing PND surgery or sham operation, focusing on astrocytes. We identified 13 distinct clusters corresponding to nine cell types, including astrocytes, microglia, neurons, oligodendrocytes, and other relevant cell populations. Specifically, five astrocyte subclusters were identified, with cluster 0 being the most abundant. Its proportion decreased by 5.51% in the PND surgery condition, showing the largest difference between the groups. Functional enrichment analysis revealed that astrocytes are involved in crucial neurodevelopmental processes and pathways associated with nervous system development and synaptic regulation. Pseudotime analysis placed cluster 0 at the early stage of differentiation, suggesting it as a key responsive population. Gene co-expression network further identified modules with peak activity in cluster 0. By intersecting cluster 0 markers with differentially expressed genes (DEGs) and applying machine learning methods, including LASSO, XGBoost, and Random Forest, we pinpointed four feature genes <i>Dbp</i>, <i>PISD</i>, <i>Id4</i>, and <i>Tsc22d3</i> with differential expression patterns between surgery and control conditions. Transcription factor activity analysis highlighted distinct regulatory networks in astrocytes, providing insights into their functional differences in response to PND surgery. These findings offer a detailed aged hippocampal landscape of astrocyte dynamics and intercellular communication, contributing to our understanding of neuroinflammation and cognitive dysfunction following surgical stress.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145272714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Antibodies Directed Against Rubella Virus Induce Demyelination in Aggregating Rat Brain Cell Cultures","authors":"","doi":"10.1002/jnr.70082","DOIUrl":"https://doi.org/10.1002/jnr.70082","url":null,"abstract":"<p>RETRACTION: C. Besson Duvanel, P. Honegger and J.-M. Matthieu, “Antibodies Directed Against Rubella Virus Induce Demyelination in Aggregating Rat Brain Cell Cultures,” <i>Journal of Neuroscience Research</i> 65, no. 5 (2001): 446-454, https://doi.org/10.1002/jnr.1173.</p><p>The above article, published online on 28 August 2001 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Lawrence S. Sherman, and Wiley Periodicals LLC. The retraction has been agreed upon following an investigation into concerns raised by a third party. The article purports a homology between amino acid sequences of myelin oligodendrocyte glycoprotein (MOG) and the rubella virus E2 glycoprotein. However, further analysis has demonstrated that the referenced sequences are not present in the mature MOG proteins. The authors did not respond to address the concerns and did not provide their original data. As a result, the editors consider the conclusions of this article to be unsupported.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 10","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70082","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Focused Ultrasound-Induced Peripheral Nerve Blockade: Duration of Changes to Thermal Withdrawal Latency and Nerve Structure After Focused Ultrasound Application to the Sciatic Nerve in a Rat Model of Acute Pain","authors":"Gwen Gao,&nbsp;Zara Thomas,&nbsp;Husniye Kantarci,&nbsp;Cholawat Pacharinsak,&nbsp;J. Bradley Zuchero,&nbsp;Kim Butts Pauly,&nbsp;David C. Yeomans,&nbsp;Thomas A. Anderson","doi":"10.1002/jnr.70079","DOIUrl":"10.1002/jnr.70079","url":null,"abstract":"<div>\u0000 \u0000 <p>Focused ultrasound (FUS) holds potential to inhibit peripheral nerves to manage pain. We previously found FUS parameters resulting in changes to nerve structure and reversible increased mechanical withdrawal threshold as well as reversible inhibition of motor and non-pain sensory fibers. However, as behaviors were only followed for 4 weeks and structure for 2 weeks, the duration of increased thermal withdrawal latency and changes to nerve structure were undetermined. We investigated the duration of increased thermal withdrawal latency and nerve structure alterations after FUS application in an acute pain model. FUS was applied directly to the rat sciatic nerve prior to hindpaw (HP) incision; animal behaviors (thermal and mechanical nociceptive thresholds, HP extension and flexion) were assessed for 12 weeks and nerve structure was assessed for 28 weeks. The primary outcome was the change in HP thermal withdrawal latency. Secondary outcomes were the changes to sciatic nerve structure and HP mechanical withdrawal threshold, extension, and flexion. Compared with controls, after FUS application, animals had increased thermal nociceptive thresholds until week 9, increased mechanical nociceptive thresholds until week 2, decreased HP motor response until week 3.5, and decreased HP plantar sensation until week 4. Nerve ultrastructure changes may have persisted until week 24. In this new longer-term follow-up study, after invasive FUS application to the sciatic nerve in a rodent model of acute incisional pain, we determined the duration of changes to thermal hyperalgesia, mechanical hyperalgesia, motor, and non-pain sensory responses, and changes to nerve structure.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combination of Treadmill Training and Inosine Enhance Nerve Regeneration and Functional Recovery After Mice Sciatic Nerve Transection","authors":"Tiago Batos Taboada,&nbsp;Luiza dos Santos Heringer,&nbsp;Camila Linhares Fernandes de Oliveira,&nbsp;Gabriel Valladares da Rosa,&nbsp;Fernanda Marques Pestana,&nbsp;Ricardo Cardoso,&nbsp;Fellipe Soares dos Santos Cardoso,&nbsp;Roberta Ramos Cavalcanti,&nbsp;Bruna dos Santos Ramalho,&nbsp;Ana Maria Blanco Martinez,&nbsp;Fernanda Martins de Almeida","doi":"10.1002/jnr.70080","DOIUrl":"10.1002/jnr.70080","url":null,"abstract":"<p>Peripheral nerve injuries are a major cause of disability, leading to significant sensorimotor impairment and functional loss. These injuries can result from traumatic or non-traumatic events, with severe cases posing therapeutic challenges. Neurorrhaphy is the gold standard for treating injuries where the gap between nerve stumps is less than 3 cm, while autografting is used for larger gaps. Despite various therapeutic approaches aimed at enhancing peripheral nerve regeneration, restoring pre-injury function remains difficult in clinical practice, prompting the exploration of experimental therapies. This study examined the effects of treadmill training and inosine treatment on sciatic nerve regeneration after transection in mice. Male C57/Bl6 mice (8–12 weeks) underwent sciatic nerve transection, with the proximal and distal stumps sutured to a polylactic acid tubular graft, creating a 3 mm gap. The mice were treated with saline or inosine (70 mg/mL) for 1 week, followed by treadmill exercise starting in the second week. The exercise protocol involved treadmill speeds of 6–12 m/min, three times per week for 10 min, continuing for 8 weeks. Functional recovery was assessed weekly using the Sciatic Functional Index, pinprick test, and Von Frey electronic analgesiometer. At the end of the study, electrophysiological tests and morphologic analysis were performed. The results showed that the combination of inosine with treadmill training significantly accelerated functional recovery and nerve regeneration, suggesting that this combined approach may offer a promising alternative for improving recovery outcomes in cases of peripheral nerve injury.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of a Ferret Model of Traumatic Brain Injury due to Under-Vehicle Blast, Controlled Cortical Impact, or Blast Plus Impact","authors":"Molly J. Goodfellow,&nbsp;Amanda L. Hrdlick,&nbsp;Boris Piskoun,&nbsp;Julie L. Proctor,&nbsp;Parisa Rangghran,&nbsp;Michael C. Shaughness,&nbsp;Alexandra Vesselinov,&nbsp;Su Xu,&nbsp;Rao P. Gullapalli,&nbsp;Ulrich H. Leiste,&nbsp;William L. Fourney,&nbsp;Catriona H. T. Miller,&nbsp;Jody C. Cantu,&nbsp;Gary Fiskum","doi":"10.1002/jnr.70081","DOIUrl":"https://doi.org/10.1002/jnr.70081","url":null,"abstract":"<p>Under-vehicle blast (UVB) generated from landmines is a unique traumatic brain injury (TBI) mechanism affecting warfighters. UVB hyperacceleration can result in injury independent of impact; however, a secondary impact injury can also occur. To date, translation of findings from rodent TBI models to improved patient outcomes has been unsuccessful, perhaps due to neuroanatomical differences between humans and rodents, including white-to-gray matter ratio and cortical gyrification. To address this modeling difference, a UVB model was developed in ferrets, the brains of which more closely resemble humans. Male ferrets underwent UVB-alone (Blast), controlled cortical impact (CCI)-alone, combined UVB + CCI (BCCI), or craniotomy (Sham) procedures. Neurobehavioral assays were optimized and used to assess mood, memory, and motor control. Blast and BCCI ferrets underwent neuroimaging at baseline and 7 days post-injury. All ferrets were euthanized by terminal perfusion with paraformaldehyde on day 7 for histologic analysis. Results indicate that UVB alters cortical metabolites and induces blood–brain barrier (BBB) disruption. CCI leads to BBB disruption and cortical diffuse axonal injury, but this is not exacerbated by combination with UVB. BCCI does result in several alterations in key cortical metabolites indicative of increased neuronal injury, oxidative stress, and glial activation as well as impaired neurotransmission and energy generation. Additionally, BCCI significantly increases hyperactivity and impairs spatial memory. Anxiety-like behavior, mood, and motor function approached statistical significance. Taken together, we provide a military-relevant model of UVB in a gyrencephalic animal, the ferret, that may be applied in future investigations into TBI pathophysiology and potential treatment.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 9","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70081","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}