Brain Research最新文献

{"title":"IGF2BP2-mediated m6A modification of IGF1R mRNA promotes neuronal senescence and cognitive decline in Alzheimer’s disease","authors":"Shan Hui ,&nbsp;Yi Long ,&nbsp;Lemei Zhu ,&nbsp;Wei Shi ,&nbsp;Qing Zheng ,&nbsp;Lihui Liang","doi":"10.1016/j.brainres.2025.150067","DOIUrl":"10.1016/j.brainres.2025.150067","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer’s disease (AD) is characterized by cognitive decline and neuronal loss, with cellular senescence emerging as a key driver. The insulin-like growth factor-1 receptor (IGF1R) pathway is implicated in aging and AD pathology. IGF2 mRNA binding protein 2 (IGF2BP2) can stabilize IGF1R mRNA, but its role in AD-associated neuronal senescence remains unclear.</div></div><div><h3>Methods</h3><div>We established AD mouse models and H₂O₂-induced senescent neuronal cell models to explore the impact of IGF2BP2 in neuronal senescence and cognitive deficits. RNA pull-down assays, methylated RNA immunoprecipitation (MeRIP)-qPCR, and behavioral tests were used to elucidate the molecular mechanisms and therapeutic potential of targeting IGF2BP2.</div></div><div><h3>Results</h3><div>IGF2BP2 was significantly up-regulated in the hippocampal neurons of AD mice. This upregulation correlated with increased β-amyloid (Aβ) deposition, neuronal damage, and cognitive impairments. In <em>vitro</em>, IGF2BP2 knockdown in H₂O₂-induced senescent neurons reduced IGF1R expression and alleviated neuronal senescence, as evidenced by decreased senescence-associated secretory phenotype factors and improved cell viability. Mechanistically, IGF2BP2 stabilized IGF1R mRNA through m6A modification, enhancing its expression. Knockdown of IGF2BP2 decreased IGF1R mRNA stability and expression, thereby mitigating neuronal senescence. In AD mice, IGF2BP2 knockdown improved cognitive function, reduced Aβ deposition, and delayed neuronal senescence.</div></div><div><h3>Conclusion</h3><div>IGF2BP2 contributes to neuronal senescence and cognitive deficits in AD by regulating IGF1R expression through m6A modification.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1871 ","pages":"Article 150067"},"PeriodicalIF":2.6,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145586208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Static and dynamic alterations in local brain activity and their association with dysfunctional connectivity in depressed adolescents with suicide attempts and non-suicidal self-injury","authors":"Lianlian Yang ,&nbsp;Shuai Wang ,&nbsp;Zimo Zhou ,&nbsp;Zhenru Guo ,&nbsp;Shuaiyi Guo ,&nbsp;Xiaoshan Gao ,&nbsp;Yuanyuan Yang ,&nbsp;Yu Xia ,&nbsp;Haixia Huang ,&nbsp;Jianhua Li ,&nbsp;Haohao Zhu ,&nbsp;Lin Tian","doi":"10.1016/j.brainres.2025.150064","DOIUrl":"10.1016/j.brainres.2025.150064","url":null,"abstract":"<div><div>Suicide attempts (SA) and non-suicidal self-injury (NSSI) are critical public health concerns that frequently co-occur in depressed adolescents. However, the neurological mechanisms underlying these behaviors remain poorly understood. This study aimed to identify alterations in brain activity and examine the associations between these changes and clinical symptom severity in depressed adolescents with SA and NSSI. A total of 82 depressed adolescents with NSSI were divided into two groups: those with both SA and NSSI (SA + NSSI, n = 46) and those with NSSI only (n = 36). Static amplitude of low-frequency fluctuation (sALFF) and dynamic ALFF variability (dALFF variability) analyses were conducted to assess local brain activity differences between groups. Regions with abnormal neural activity were used as seeds to investigate static functional connectivity (sFC) and dynamic FC variability (dFC variability) alterations. Correlation analyses as exploratory analysis was subsequently performed. Compared to the NSSI group, the SA + NSSI group exhibited increased sALFF in the left cerebellum, increased dALFF variability in the orbitofrontal cortex and left cerebellum, and increased dFC variability between the orbitofrontal cortex and caudate. The SA + NSSI group also showed decreased sALFF and dALFF variability in the postcentral gyrus (cluster <em>p</em> &lt; 0.05, FDR corrected, two-tailed). Additionally, for the SA + NSSI group, sALFF in the postcentral gyrus was negatively correlated with emotional neglect, while the dFC variability between the orbitofrontal cortex and caudate was positively correlated with internet addiction withdrawal symptoms. These findings provide novel insights into the neurological mechanisms of SA and NSSI, highlighting the potential value of combining static and dynamic functional metrics for clinical differentiation between these behaviors.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1871 ","pages":"Article 150064"},"PeriodicalIF":2.6,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145652946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DDX3X promotes ILF3 stability to accelerate neuroblastoma progression via M2 macrophage polarization","authors":"Tian Lin,&nbsp;Xinghe Chen,&nbsp;He Huang,&nbsp;Jianxing Zhang,&nbsp;Junshan Lin","doi":"10.1016/j.brainres.2025.150071","DOIUrl":"10.1016/j.brainres.2025.150071","url":null,"abstract":"<div><div>Neuroblastoma (NB) is a common pediatric solid tumor with poor prognosis, in which macrophage polarization is increasingly recognized as a key driver of progression. However, the roles of RNA-binding proteins such as DEAD-box helicase 3 X-linked (DDX3X) and interleukin enhancer-binding factor 3 (ILF3) in this process remain unclear. This study aims to explore the role of the DDX3X–ILF3 axis in modulating macrophage polarization and promoting the malignant progression of NB. ILF3 expression was analyzed by RT-qPCR and Western blotting. Lentiviral-mediated knockdown of ILF3 or DDX3X was performed, followed by evaluation of cell viability, proliferation, invasion, and migration, respectively. In a Transwell co-culture system, the expression of polarization markers was examined by Western blotting, and the secretion of inflammatory cytokines was measured by enzyme-linked immunosorbent assay. Actinomycin D treatment combined with RT-qPCR was used to assess ILF3 mRNA stability. RIP-qPCR was employed to explore the interaction of DDX3X with ILF3 mRNA. NB xenograft and metastasis mouse model (lung, liver, and kidney) was established to evaluate the regulatory effects of the DDX3X inhibitor RK-33 and ILF3 overexpression on NB growth and metastasis. ILF3 expression was significantly upregulated in NB cells. Knockdown of ILF3 or DDX3X suppressed NB cell viability, proliferation, invasion, and migration, while promoting M1 macrophage polarization accompanied by increased secretion of inflammatory cytokines. Silencing DDX3X reduced ILF3 mRNA stability and protein expression, whereas ILF3 overexpression negated the suppressive impacts of DDX3X knockdown on malignant behaviors and polarization status. <em>In vivo</em>, DDX3X inhibitor, RK-33, markedly inhibited NB tumor growth and metastasis and enhanced M1 macrophage polarization, which was partially reversed by ILF3 overexpression. DDX3X promotes NB progression by stabilizing ILF3 mRNA, thereby facilitating M2 macrophage polarization.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1871 ","pages":"Article 150071"},"PeriodicalIF":2.6,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145622786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Volume current coupling—remote direct neural coupling across the extracellular space","authors":"Ayumu Matani ,&nbsp;Yusuke Takeda ,&nbsp;Motofumi Fushimi ,&nbsp;Akira Tsukamura","doi":"10.1016/j.brainres.2025.150066","DOIUrl":"10.1016/j.brainres.2025.150066","url":null,"abstract":"<div><div>Although electrical devices should not be submerged, the brain, despite its electrical implementation, is submerged in an electrolyte solution and has indeed leakage currents as demonstrated by electroencephalograms (EEGs). Ephaptic coupling is a direct electrical neural coupling mediated by leakage currents between adjacent neurons on a microscale, and it affects spike timing. Since EEGs are detectable, meaning that tens of thousands of neurons activate synchronously, their collective leakage currents can extend the coupling over longer distances, hereafter called volume current coupling (VcC). Here, we show neural coupling (NC) = synaptic coupling (SC) + VcC and find a function of VcC. When two people, sensorily isolated but electrically connected at the heads in a skillful way to exchange their volume currents (Vcs) to avoid attenuation, were given separate left–right discrimination tasks, a significant conflict, or a task-irrelevant conditional bias, occurred in the discrimination. No SC existed between the two participants, indicating a behaviorally functional VcC. The Vc propagation path contains neurons of the person producing the Vc, and intra-person VcCs can also occur. In fact, as intra-person effects, an unconditional right-preferential bias emerged when electrically disconnected, but a task-irrelevant conditional right-preferential bias, or priming, emerged when connected. Since the skillful connection intervenes only in VcC, NC = SC + VcC is true also in individual brains and one function of VcC is to generate these biases. Since VcCs are ubiquitous in the brain as electrical crosstalk, it may be better not to study cognitive and behavioral functions in the SC alone.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1871 ","pages":"Article 150066"},"PeriodicalIF":2.6,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145602287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between ApoE-expressing cells and genotoxic stress in the mouse brain","authors":"Ummay Ayman ,&nbsp;Takayoshi Otsuka ,&nbsp;Godfried Dougnon ,&nbsp;Hideaki Matsui","doi":"10.1016/j.brainres.2025.150080","DOIUrl":"10.1016/j.brainres.2025.150080","url":null,"abstract":"<div><div>Apolipoprotein E (ApoE) plays an important role in cerebral lipid transport. Beyond lipid transport, ApoE also contributes to the maintenance of neuronal integrity. Although DNA damage and dysfunction in the DNA damage response are recognized as early contributors to neuropathology, the connection between ApoE and DNA damage remains poorly understood. In this study, we investigated cells expressing endogenous mouse ApoE (mApoE) in the brain under both normal condition and etoposide-induced DNA damage. Immunohistochemical analysis revealed that mApoE was predominantly expressed in astrocytes and a subset of neurons across various brain regions, with minimal expression in microglia and no detectable expression in oligodendrocytes. Induction of DNA damage through etoposide treatment did not alter the expression level or distribution pattern of mApoE in brain. However, a correlation between neuronal mApoE expression and DNA damage was observed: mApoE-positive neurons were more affected and exhibited a higher number of γH2A.X foci upon etoposide treatment. This observation warrants further investigation to determine whether the increased sensitivity of mApoE-positive neurons to DNA damage is neuroprotective or contributes to neurodegeneration. Our study provides a foundation for understanding the physiological role of mApoE in response to DNA damage and suggests a potential involvement of neuronal mApoE in neurodegeneration.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1871 ","pages":"Article 150080"},"PeriodicalIF":2.6,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145629620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondria serve as indispensable components of neuron-glia crosstalk in the trajectory of Alzheimer’s disease","authors":"Maryam Sardari ,&nbsp;Oveis Hosseinzadeh Sahafi ,&nbsp;Ameneh Rezayof","doi":"10.1016/j.brainres.2025.150040","DOIUrl":"10.1016/j.brainres.2025.150040","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is a multiplex and progressive neurodegenerative disorder commonly recognized by the accumulation of amyloid-β (Aβ) plaques, neurofibrillary tangles (NFTs), and dysfunction in the cholinergic and glutamatergic systems. At the early stages of AD, mitochondrion operates as a neuroprotective organelle in both neuronal and glial cells by compensating energy fluctuations. As the disease progresses, mitochondrial function in both neurons and glial cells deteriorates, culminating in impaired cellular metabolism and glial hyperactivation. This time-dependent hyperactivation of microglia and astrocytes sequentially promotes the release of pro-inflammatory cytokines, elevates reactive oxygen species, disrupts calcium homeostasis, and increases oxidative stress. Altogether, these processes drive neuroinflammation, which both influences and is influenced by mitochondrial activity. Additionally, mitochondrial dysfunction across the disease trajectory hampers communication between neurons and glial cells, promoting excitotoxicity in neurons. This review emphasizes the vital role of mitochondrial dynamics in AD pathophysiology across different stages and explores how cell-specific targeting of mitochondrial activity could mitigate neuroinflammation, restore neuronal function, and offer potential treatment benefits. Enhancing mitochondrial function in healthy neurons and glial cells, particularly in microglia as a compensatory mechanism, especially at the early stage of the disease or restoring mitochondrial function of surviving neurons at the later stages, may promote neuroprotection and improve neuron-glia interactions, thus offering a potential strategy for AD treatment.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1870 ","pages":"Article 150040"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145562825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of concern: “Protective effects of propofol against whole cerebral ischemia/reperfusion injury in rats through the inhibition of the apoptosis-inducing factor pathway” [Brain Res. 1644 (2016) 9–14]","authors":"Tao Tao ,&nbsp;Chun-lei Li ,&nbsp;Wan-chao Yang,&nbsp;Xian-zhang Zeng,&nbsp;Chun-yu Song,&nbsp;Zi-yong Yue,&nbsp;Hong Dong,&nbsp;Hua Qian","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1885 ","pages":"Article 150345"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147860556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cross-frequency brain functional network analysis of auditory stimulation in acute disorders of consciousness","authors":"Ning Yin ,&nbsp;Jing Zhao ,&nbsp;Haili Wang ,&nbsp;Junqing Zhang ,&nbsp;Guizhi Xu ,&nbsp;Zhongzhen Li ,&nbsp;Guobin Zhang","doi":"10.1016/j.brainres.2025.150043","DOIUrl":"10.1016/j.brainres.2025.150043","url":null,"abstract":"<div><div>Currently, prognostic assessment for patients with acute disorders of consciousness (DOC) remains a key and challenging focus in neuroscience. Existing research has predominantly concentrated on brain functional connectivity within specific frequency bands, overlooking the potential role of cross-frequency coupling (CFC). To address this, this study systematically analyzed within-frequency coupling (WFC) and CFC in 38 patients with acute DOC (18 cases transitioning to minimally conscious state (MCS) and 20 cases to vegetative state (VS) in the prolonged phase) based on electroencephalogram (EEG) signals recorded during auditory name‑calling stimulation. Furthermore, WFC brain networks and two‑layer functional brain networks incorporating both WFC and CFC were constructed to investigate their association with consciousness prognosis. The results revealed that, compared to the VS group, the MCS group exhibited significantly stronger WFC in the alpha band but significantly weaker WFC in the delta and theta bands, as well as reduced delta–theta and theta–beta CFC. These differences were more pronounced in the frontal‑parietal regions. Graph theoretical analysis indicated that the MCS group exhibited significantly higher small‑world properties in the alpha band and the cross-frequency theta–beta and alpha–beta networks, suggesting better‑preserved information processing efficiency in their brain networks. These findings demonstrate that CFC and multilayer network topological properties hold significant potential in characterizing the level of consciousness in acute DOC, and may offer new electrophysiological insights for early prognostic evaluation.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1870 ","pages":"Article 150043"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145494532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inherited and seizure-induced abnormalities in the temporal cortex astroglia of Krushinsky-Molodkina audiogenic rats: A pilot study","authors":"Yulia S. Grigorieva,&nbsp;Ksenia A. Ivanova,&nbsp;Elena V. Chernigovskaya,&nbsp;Alexandra A. Naumova,&nbsp;Margarita V. Glazova","doi":"10.1016/j.brainres.2025.150056","DOIUrl":"10.1016/j.brainres.2025.150056","url":null,"abstract":"<div><div>The role of astrocytes in the pathogenesis of temporal lobe epilepsy (TLE) is intensively studied. Here, we present a pilot study of astrocytes in the temporal cortex of Krushinsky-Molodkina (KM) rats, which are genetically prone to audiogenic seizures (AGS) and may be used as a model of TLE when exposed to audiogenic kindling. Naïve KM rats (with no AGS) were compared to Wistar rats to disclose the inherited abnormalities, and KM rats after 14-day audiogenic kindling were compared to naïve ones to determine TLE effects. Our results demonstrated that in the temporal cortex of naïve KM rats, the population of ALDH1L1-positive astrocytes was unaltered, while GFAP-positive astrocytes were localized only in the outer layers. Nuclear factor IA (NFIA)-positive astrocytes were distributed evenly, but their number was also lower. In addition, decreased aquaporin 4 and Kir4.1 were revealed indicating defective water and potassium homeostasis. These data point on genetically determined disfunction of cortex astroglia associated with inherited epileptic predisposition. After audiogenic kindling, KM rats still demonstrated no changes in ALDH1L1 expression, however, exhibited increased number of NFIA-positive astrocytes in the temporal cortex and upregulation of GFAP, aldolase C, and glutamine synthetase. Meanwhile, kindling further exacerbated the basal deficits of aquaporin 4 and Kir4.1.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1870 ","pages":"Article 150056"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145522765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synaptic function of descending projections from the insular cortex to the nucleus solitary tract in the rat","authors":"Ami Wakabayashi ,&nbsp;Yuka Nakaya ,&nbsp;Kiyofumi Yamamoto ,&nbsp;Yumi Tsutsumi ,&nbsp;Fumihiko Sato ,&nbsp;Atsushi Yoshida ,&nbsp;Takashi Kikuiri ,&nbsp;Masayuki Kobayashi","doi":"10.1016/j.brainres.2025.150061","DOIUrl":"10.1016/j.brainres.2025.150061","url":null,"abstract":"<div><div>The rostral part of the nucleus of the solitary tract (rNST) receives gustatory inputs via the facial, glossopharyngeal, and vagus nerves. In addition to these ascending pathways, the rNST receives descending projections from higher brain regions, including the insular cortex (IC). Neurons in the dysgranular and granular IC around the middle cerebral artery (MCA) respond to gustatory stimulation; therefore, descending IC projections to the rNST are thought to regulate gustatory information processing. However, little is known about how IC inputs modulate rNST neuronal activity at the synaptic level, which comprises both glutamatergic and GABAergic neurons. In this study, we examined the synaptic strength of IC → rNST projections in glutamatergic and GABAergic neurons using vesicular GABA transporter–Venus transgenic rats. We first confirmed that the IC subregion around the MCA, a region where gustatory information converges, projects axons to the rNST. Whole-cell patch-clamp recordings revealed that rNST neurons could be classified into three groups: regular-spiking (68.2 %), late-spiking (22.7 %), and burst-spiking (9.1 %). Among glutamatergic neurons, 58.8 % were regular-spiking, 23.5 % were late-spiking, and 17.6 % were burst-spiking, whereas GABAergic neurons were predominantly regular-spiking (77.8 %), with fewer late-spiking (18.5 %) and burst-spiking (3.7 %) neurons. In rats injected with AAV5-CAG-ChR2(H134R)-mCherry into the IC subregion, both glutamatergic and GABAergic rNST neurons exhibited photostimulation-induced monosynaptic excitatory postsynaptic currents with comparable amplitudes and latencies. Paired whole-cell recordings further demonstrated that glutamatergic neurons receive inhibitory inputs from rNST GABAergic neurons with a high failure rate. These findings suggest that IC projections to the rNST primarily enhance excitatory output from the rNST neurons. (250/250 words)</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1870 ","pages":"Article 150061"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145556283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}