Molecular Brain最新文献_第10页

Intraplantar aminoglutethimide, a P450scc inhibitor, reduced the induction of mechanical allodynia in a rat model of thrombus-induced ischemic pain. 在血栓诱发缺血性疼痛的大鼠模型中，P450scc抑制剂氨鲁米特可减少机械异感的诱导。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-08-02 DOI: 10.1186/s13041-024-01125-2

Soon-Gu Kwon, Hoon-Seong Choi, Seo-Yeon Yoon, Dae-Hyun Roh, Jang-Hern Lee

{"title":"Intraplantar aminoglutethimide, a P450scc inhibitor, reduced the induction of mechanical allodynia in a rat model of thrombus-induced ischemic pain.","authors":"Soon-Gu Kwon, Hoon-Seong Choi, Seo-Yeon Yoon, Dae-Hyun Roh, Jang-Hern Lee","doi":"10.1186/s13041-024-01125-2","DOIUrl":"10.1186/s13041-024-01125-2","url":null,"abstract":"Neuroactive steroids (NASs) directly affect neuronal excitability. Despite their role in the nervous system is intimately linked to pain control, knowledge is currently limited. This study investigates the peripheral involvement of NASs in chronic ischemic pain by targeting the cytochrome P450 side-chain cleavage enzyme (P450scc). Using a rat model of hind limb thrombus-induced ischemic pain (TIIP), we observed an increase in P450scc expression in the ischemic hind paw skin. Inhibiting P450scc with intraplantar aminoglutethimide (AMG) administration from post-operative day 0 to 3 significantly reduced the development of mechanical allodynia. However, AMG administration from post-operative day 3 to 6 did not affect established mechanical allodynia. In addition, we explored the role of the peripheral sigma-1 receptor (Sig-1R) by co-administering PRE-084 (PRE), a Sig-1R agonist, with AMG. PRE reversed the analgesic effects of AMG during the induction phase. These findings indicate that inhibiting steroidogenesis with AMG alleviates peripheral ischemic pain during the induction phase via Sig-1Rs.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"50"},"PeriodicalIF":3.3,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11295590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879113","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}

引用次数: 0

Neurexin-3 in the paraventricular nucleus of the hypothalamus regulates body weight and glucose homeostasis independently of food intake. 下丘脑室旁核中的 Neurexin-3 与食物摄入无关，可调节体重和葡萄糖稳态。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-08-01 DOI: 10.1186/s13041-024-01124-3

Mingdao Mu, Haoyu Sun, Shuyan Geng, Tianxiang Xu, Chuanyao Sun, Zixu Zhang, Sibie Meng, Moyi Li, An Liu, Zhiyuan Yang, Wei Xie

{"title":"Neurexin-3 in the paraventricular nucleus of the hypothalamus regulates body weight and glucose homeostasis independently of food intake.","authors":"Mingdao Mu, Haoyu Sun, Shuyan Geng, Tianxiang Xu, Chuanyao Sun, Zixu Zhang, Sibie Meng, Moyi Li, An Liu, Zhiyuan Yang, Wei Xie","doi":"10.1186/s13041-024-01124-3","DOIUrl":"10.1186/s13041-024-01124-3","url":null,"abstract":"Neurexin-3 (Nrxn3) has been genetically associated with obesity, but the underlying neural mechanisms remain poorly understood. This study aimed to investigate the role of Nrxn3 in the paraventricular nucleus of the hypothalamus (PVN) in regulating energy balance and glucose homeostasis. We found that Nrxn3 expression in the PVN was upregulated in response to metabolic stressors, including cold exposure and fasting. Using Cre-loxP technology, we selectively ablated Nrxn3 in CaMKIIα-expressing neurons of the PVN in male mice. This genetic manipulation resulted in marked weight gain attributable to increased adiposity and impaired glucose tolerance, without affecting food intake. Our findings identify PVN CaMKIIα-expressing neurons as a critical locus where Nrxn3 modulates energy balance by regulating adipogenesis and glucose metabolism, independently of appetite. These results reveal a novel neural mechanism potentially linking Nrxn3 dysfunction to obesity pathogenesis, suggesting that targeting PVN Nrxn3-dependent neural pathways may inform new therapeutic approaches for obesity prevention and treatment.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"49"},"PeriodicalIF":3.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11295692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875361","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}

引用次数: 0

Systemic inflammation attenuates the repair of damaged brains through reduced phagocytic activity of monocytes infiltrating the brain. 全身性炎症会降低浸润大脑的单核细胞的吞噬活性，从而削弱受损大脑的修复能力。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-07-29 DOI: 10.1186/s13041-024-01116-3

Sushil Gaire, Jiawei An, Haijie Yang, Keon Ah Lee, Manisha Dumre, Eun Jeong Lee, Sang-Myun Park, Eun-Hye Joe

{"title":"Systemic inflammation attenuates the repair of damaged brains through reduced phagocytic activity of monocytes infiltrating the brain.","authors":"Sushil Gaire, Jiawei An, Haijie Yang, Keon Ah Lee, Manisha Dumre, Eun Jeong Lee, Sang-Myun Park, Eun-Hye Joe","doi":"10.1186/s13041-024-01116-3","DOIUrl":"10.1186/s13041-024-01116-3","url":null,"abstract":"In this study, we examined how systemic inflammation affects repair of brain injury. To this end, we created a brain-injury model by stereotaxic injection of ATP, a damage-associated molecular pattern component, into the striatum of mice. Systemic inflammation was induced by intraperitoneal injection of lipopolysaccharide (LPS-ip). An analysis of magnetic resonance images showed that LPS-ip reduced the initial brain injury but slowed injury repair. An immunostaining analysis using the neuronal marker, NeuN, showed that LPS-ip delayed removal of dead/dying neurons, despite the fact that LPS-ip enhanced infiltration of monocytes, which serve to phagocytize dead cells/debris. Notably, infiltrating monocytes showed a widely scattered distribution. Bulk RNAseq analyses showed that LPS-ip decreased expression of genes associated with phagocytosis, with PCR and immunostaining of injured brains confirming reduced levels of Cd68 and Clec7a, markers of phagocytic activity, in monocytes. Collectively, these results suggest that systemic inflammation affects properties of blood monocytes as well as brain cells, resulting in delay in clearing damaged cells and activating repair processes.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"47"},"PeriodicalIF":3.3,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11288066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792929","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}

引用次数: 0

β-hydroxybutyrate and ischemic stroke: roles and mechanisms. β-羟丁酸与缺血性中风：作用与机制。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-07-29 DOI: 10.1186/s13041-024-01119-0

Ge Feng, Zongkai Wu, Leyi Yang, Kaimeng Wang, Hebo Wang

引用次数: 0

Spared nerve injury leads to reduced activity of neurons projecting from the ventrolateral periaqueductal gray to the locus coeruleus. 幸免神经损伤会导致从腹外侧下腹灰质投射到神经节的神经元活动减弱。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-07-24 DOI: 10.1186/s13041-024-01121-6

Wing Lam Yu, Zizhen Zhang, Gerald W Zamponi

{"title":"Spared nerve injury leads to reduced activity of neurons projecting from the ventrolateral periaqueductal gray to the locus coeruleus.","authors":"Wing Lam Yu, Zizhen Zhang, Gerald W Zamponi","doi":"10.1186/s13041-024-01121-6","DOIUrl":"10.1186/s13041-024-01121-6","url":null,"abstract":"The ventrolateral periaqueductal gray (vlPAG) serves as a central hub for descending pain modulation. It receives upstream projections from the medial prefrontal cortex (mPFC) and the ventrolateral orbitofrontal cortex (vlOFC), and projects downstream to the locus coeruleus (LC) and the rostroventral medulla (RVM). While much research has focused on upstream circuits and the LC-RVM connection, less is known about the PAG-LC circuit and its involvement in neuropathic pain. Here we examined the intrinsic electrophysiological properties of vlPAG-LC projecting neurons in Sham and spared nerve injury (SNI) operated mice. Injection of the retrotracer Cholera Toxin Subunit B (CTB-488) into the LC allowed the identification of LC-projecting neurons in the vlPAG. Electrophysiological recordings from CTB-488 positive cells revealed that both GABAergic and glutamatergic cells that project to the LC exhibited reduced intrinsic excitability after peripheral nerve injury. By contrast, CTB-488 negative cells did not exhibit alterations in firing properties after SNI surgery. An SNI-induced reduction of LC projecting cells was confirmed with c-fos labeling. Hence, SNI induces plasticity changes in the vlPAG that are consistent with a reduction in the descending modulation of pain signals.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"46"},"PeriodicalIF":3.3,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759836","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}

引用次数: 0

The myelin water imaging transcriptome: myelin water fraction regionally varies with oligodendrocyte-specific gene expression. 髓鞘水成像转录组：髓鞘水部分随少突胶质细胞特异性基因表达的区域变化而变化。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-07-23 DOI: 10.1186/s13041-024-01115-4

Jaimie J Lee, Paulina S Scheuren, Hanwen Liu, Ryan W J Loke, Cornelia Laule, Catrina M Loucks, John L K Kramer

{"title":"The myelin water imaging transcriptome: myelin water fraction regionally varies with oligodendrocyte-specific gene expression.","authors":"Jaimie J Lee, Paulina S Scheuren, Hanwen Liu, Ryan W J Loke, Cornelia Laule, Catrina M Loucks, John L K Kramer","doi":"10.1186/s13041-024-01115-4","DOIUrl":"10.1186/s13041-024-01115-4","url":null,"abstract":"Identifying sensitive and specific measures that can quantify myelin are instrumental in characterizing microstructural changes in neurological conditions. Neuroimaging transcriptomics is emerging as a valuable technique in this regard, offering insights into the molecular basis of promising candidates for myelin quantification, such as myelin water fraction (MWF). We aimed to demonstrate the utility of neuroimaging transcriptomics by validating MWF as a myelin measure. We utilized data from a normative MWF brain atlas, comprised of 50 healthy subjects (mean age = 25 years, range = 17-42 years) scanned at 3 Tesla. Magnetic resonance imaging data included myelin water imaging to extract MWF and T1 anatomical scans for image registration and segmentation. We investigated the inter-regional distributions of gene expression data from the Allen Human Brain Atlas in conjunction with inter-regional MWF distribution patterns. Pearson correlations were used to identify genes with expression profiles mirroring MWF. The Single Cell Type Atlas from the Human Protein Atlas was leveraged to classify genes into gene sets with high cell type specificity, and a control gene set with low cell type specificity. Then, we compared the Pearson correlation coefficients for each gene set to determine if cell type-specific gene expression signatures correlate with MWF. Pearson correlation coefficients between MWF and gene expression for oligodendrocytes and adipocytes were significantly higher than for the control gene set, whereas correlations between MWF and inhibitory/excitatory neurons were significantly lower. Our approach in integrating transcriptomics with neuroimaging measures supports an emerging technique for understanding and validating MRI-derived markers such as MWF.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"45"},"PeriodicalIF":3.3,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11264438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141752162","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}

引用次数: 0

The duality of amyloid-β: its role in normal and Alzheimer's disease states. 淀粉样蛋白-β的双重性：它在正常状态和阿尔茨海默病状态中的作用。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-07-17 DOI: 10.1186/s13041-024-01118-1

Ali Azargoonjahromi

{"title":"The duality of amyloid-β: its role in normal and Alzheimer's disease states.","authors":"Ali Azargoonjahromi","doi":"10.1186/s13041-024-01118-1","DOIUrl":"10.1186/s13041-024-01118-1","url":null,"abstract":"Alzheimer's disease (AD) is a degenerative neurological condition that gradually impairs cognitive abilities, disrupts memory retention, and impedes daily functioning by impacting the cells of the brain. A key characteristic of AD is the accumulation of amyloid-beta (Aβ) plaques, which play pivotal roles in disease progression. These plaques initiate a cascade of events including neuroinflammation, synaptic dysfunction, tau pathology, oxidative stress, impaired protein clearance, mitochondrial dysfunction, and disrupted calcium homeostasis. Aβ accumulation is also closely associated with other hallmark features of AD, underscoring its significance. Aβ is generated through cleavage of the amyloid precursor protein (APP) and plays a dual role depending on its processing pathway. The non-amyloidogenic pathway reduces Aβ production and has neuroprotective and anti-inflammatory effects, whereas the amyloidogenic pathway leads to the production of Aβ peptides, including Aβ40 and Aβ42, which contribute to neurodegeneration and toxic effects in AD. Understanding the multifaceted role of Aβ, particularly in AD, is crucial for developing effective therapeutic strategies that target Aβ metabolism, aggregation, and clearance with the aim of mitigating the detrimental consequences of the disease. This review aims to explore the mechanisms and functions of Aβ under normal and abnormal conditions, particularly in AD, by examining both its beneficial and detrimental effects.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"44"},"PeriodicalIF":3.3,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11256416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141633977","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}

引用次数: 0

The overexpression of DSP1 in neurons induces neuronal dysfunction and neurodegeneration phenotypes in Drosophila. 神经元中 DSP1 的过表达会诱导果蝇出现神经元功能障碍和神经退化表型。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-07-13 DOI: 10.1186/s13041-024-01117-2

Si-Eun Baek, Younghwi Kwon, Jong-Won Yoon, Hyo-Sung Kim, Jae-Yoon Yang, Dong-Seok Lee, Eunbyul Yeom

{"title":"The overexpression of DSP1 in neurons induces neuronal dysfunction and neurodegeneration phenotypes in Drosophila.","authors":"Si-Eun Baek, Younghwi Kwon, Jong-Won Yoon, Hyo-Sung Kim, Jae-Yoon Yang, Dong-Seok Lee, Eunbyul Yeom","doi":"10.1186/s13041-024-01117-2","DOIUrl":"10.1186/s13041-024-01117-2","url":null,"abstract":"Dorsal switch protein 1(DSP1), a mammalian homolog of HMGB1, is firstly identified as a dorsal co-repressor in 1994. DSP1 contains HMG-box domain and functions as a transcriptional regulator in Drosophila melanogaster. It plays a crucial role in embryonic development, particularly in dorsal-ventral patterning during early embryogenesis, through the regulation of gene expression. Moreover, DSP1 is implicated in various cellular processes, including cell fate determination and tissue differentiation, which are essential for embryonic development. While the function of DSP1 in embryonic development has been relatively well-studied, its role in the adult Drosophila brain remains less understood. In this study, we investigated the role of DSP1 in the brain by using neuronal-specific DSP1 overexpression flies. We observed that climbing ability and life span are decreased in DSP1-overexpressed flies. Furthermore, these flies demonstrated neuromuscular junction (NMJ) defect, reduced eye size and a decrease in tyrosine hydroxylase (TH)-positive neurons, indicating neuronal toxicity induced by DSP1 overexpression. Our data suggest that DSP1 overexpression leads to neuronal dysfunction and toxicity, positioning DSP1 as a potential therapeutic target for neurodegenerative diseases.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"43"},"PeriodicalIF":3.3,"publicationDate":"2024-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11245852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141603899","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}

引用次数: 0

MicroRNAs as the pivotal regulators of Temozolomide resistance in glioblastoma. 微RNA是胶质母细胞瘤中替莫唑胺耐药性的关键调节因子。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-07-02 DOI: 10.1186/s13041-024-01113-6

Mahsa Palizkaran Yazdi, Amirhosein Barjasteh, Meysam Moghbeli

{"title":"MicroRNAs as the pivotal regulators of Temozolomide resistance in glioblastoma.","authors":"Mahsa Palizkaran Yazdi, Amirhosein Barjasteh, Meysam Moghbeli","doi":"10.1186/s13041-024-01113-6","DOIUrl":"10.1186/s13041-024-01113-6","url":null,"abstract":"Glioblastoma (GBM) is an aggressive nervous system tumor with a poor prognosis. Although, surgery, radiation therapy, and chemotherapy are the current standard protocol for GBM patients, there is still a poor prognosis in these patients. Temozolomide (TMZ) as a first-line therapeutic agent in GBM can easily cross from the blood-brain barrier to inhibit tumor cell proliferation. However, there is a high rate of TMZ resistance in GBM patients. Since, there are limited therapeutic choices for GBM patients who develop TMZ resistance; it is required to clarify the molecular mechanisms of chemo resistance to introduce the novel therapeutic targets. MicroRNAs (miRNAs) regulate chemo resistance through regulation of drug metabolism, absorption, DNA repair, apoptosis, and cell cycle. In the present review we discussed the role of miRNAs in TMZ response of GBM cells. It has been reported that miRNAs mainly induced TMZ sensitivity by regulation of signaling pathways and autophagy in GBM cells. Therefore, miRNAs can be used as the reliable diagnostic/prognostic markers in GBM patients. They can also be used as the therapeutic targets to improve the TMZ response in GBM cells.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"42"},"PeriodicalIF":3.3,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11218189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492674","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}

引用次数: 0

Cerebellar damage with inflammation upregulates oxytocin receptor expression in Bergmann Glia. 炎症导致的小脑损伤会上调伯格曼胶质细胞中催产素受体的表达。

IF 3.3 3区医学

Molecular Brain Pub Date : 2024-06-28 DOI: 10.1186/s13041-024-01114-5

Ayumu Inutsuka, Aisa Hattori, Masahide Yoshida, Yuki Takayanagi, Tatsushi Onaka

{"title":"Cerebellar damage with inflammation upregulates oxytocin receptor expression in Bergmann Glia.","authors":"Ayumu Inutsuka, Aisa Hattori, Masahide Yoshida, Yuki Takayanagi, Tatsushi Onaka","doi":"10.1186/s13041-024-01114-5","DOIUrl":"https://doi.org/10.1186/s13041-024-01114-5","url":null,"abstract":"The cerebellum plays an important role in cognitive and social functioning. Childhood damage in the cerebellum increases the risk of autism spectrum disorder. Cerebellar inflammation induces social avoidance in mice. Oxytocin regulates social relationship and expression pattern of the oxytocin receptor in the brain is related to social behaviors. However, the expression patterns of the oxytocin receptor in the cerebellum remain controversial. Here, we report that the expression patterns of the oxytocin receptor in the cerebellum are highly variable among knock-in transgenic lines. We used Oxtr-Cre knock-in mice combined with a fluorescent reporter line and found that oxytocin receptor expression in Bergmann glia was more variable than that in Purkinje cells. We found that physical damage with inflammation induced the selective upregulation of the oxytocin receptor in Bergmann glia. Our findings indicate high variability in oxytocin receptor expression in the cerebellum and suggest that the oxytocin receptor can affect neural processing in pathological conditions, such as inflammation.","PeriodicalId":18851,"journal":{"name":"Molecular Brain","volume":"17 1","pages":"41"},"PeriodicalIF":3.3,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141469593","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}

引用次数: 0