Experimental Neurobiology最新文献

MCHR1 in Both Dopaminergic Neurons and Astrocytes in the SNpc Contributes to Acupuncture's Anti-Parkinsonian Effects. SNpc中多巴胺能神经元和星形胶质细胞中的MCHR1参与了针灸的抗帕金森效应

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-05-06 DOI: 10.5607/en26012

Hyowon Lee, Ju-Young Oh, Heesu Na, Mijin Yun, Jae-Nam Park, Hi-Joon Park, Min-Ho Nam

{"title":"MCHR1 in Both Dopaminergic Neurons and Astrocytes in the SNpc Contributes to Acupuncture's Anti-Parkinsonian Effects.","authors":"Hyowon Lee, Ju-Young Oh, Heesu Na, Mijin Yun, Jae-Nam Park, Hi-Joon Park, Min-Ho Nam","doi":"10.5607/en26012","DOIUrl":"https://doi.org/10.5607/en26012","url":null,"abstract":"Acupuncture stimulation at the GB34 acupoint has been reported to alleviate motor dysfunction in Parkinson's disease (PD) by activating the lateral hypothalamic melanin concentrating hormone (MCH) neurons projecting to the substantia nigra pars compacta (SNpc). MCH receptor 1 (MCHR1) signaling is also known to be essential for the anti-Parkinsonian effects of acupuncture. However, the cellular distribution of MCHR1 and its cell type-specific contributions to the therapeutic effects of acupuncture in PD remain largely unexplored. Here, we show that MCHR1 is expressed in both dopaminergic neurons and astrocytes within the SNpc, with higher expression in dopaminergic neurons. We further demonstrate that cell-type-specific gene-silencing of MCHR1 in either dopaminergic neurons or astrocytes significantly blocks acupuncture-induced motor recovery and dopaminergic neuron protection. These findings indicate that both neuronal and astrocytic MCHR1 contribute to the anti-Parkinsonian effects of acupuncture. Together, this study provides new insight into MCHR1 as a potential therapeutic target for PD.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835823","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}

引用次数: 0

Repeated Intra-cisterna Magna Injections with Amyloid-beta Oligomers to Induce Alzheimer's Disease in Cynomolgus Monkey (Macaca fascicularis): A Pilot Study. 大池内反复注射β淀粉样蛋白寡聚物诱导食蟹猴阿尔茨海默病：一项初步研究。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-05-06 DOI: 10.5607/en25052

Jiyeon Cho, Jinyoung Won, Yu Gyeong Kim, Chang-Yeop Jeon, Kyung Seob Lim, Jincheol Seo, Jung Bae Seong, Hyeon-Gu Yeo, Keonwoo Kim, Minji Kim, Lee Wha Gwon, Yunkyo Jung, Thanh Thi Hai Nguyen, Jisun Min, Gahye Moon, Won Seok Choi, Sung-Hyun Park, Hwal-Yong Lee, Kang-Jin Jeong, Gyu-Seo Bae, Eunsu Jeon, Da Yeon Cheong, Gyudo Lee, Hyoung-Chin Kim, Eunha Baeg, Sunggu Yang, Jae-Won Huh, Junghyung Park, Youngjeon Lee

{"title":"Repeated Intra-cisterna Magna Injections with Amyloid-beta Oligomers to Induce Alzheimer's Disease in Cynomolgus Monkey (Macaca fascicularis): A Pilot Study.","authors":"Jiyeon Cho, Jinyoung Won, Yu Gyeong Kim, Chang-Yeop Jeon, Kyung Seob Lim, Jincheol Seo, Jung Bae Seong, Hyeon-Gu Yeo, Keonwoo Kim, Minji Kim, Lee Wha Gwon, Yunkyo Jung, Thanh Thi Hai Nguyen, Jisun Min, Gahye Moon, Won Seok Choi, Sung-Hyun Park, Hwal-Yong Lee, Kang-Jin Jeong, Gyu-Seo Bae, Eunsu Jeon, Da Yeon Cheong, Gyudo Lee, Hyoung-Chin Kim, Eunha Baeg, Sunggu Yang, Jae-Won Huh, Junghyung Park, Youngjeon Lee","doi":"10.5607/en25052","DOIUrl":"https://doi.org/10.5607/en25052","url":null,"abstract":"Alzheimer's disease (AD) is a progressive neurodegenerative disorder which results in cognitive decline and memory loss, characterized by the accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles in the brain. Despite numerous efforts to develop animal models of AD across various species to understand its pathological characteristics and underlying mechanisms, the model that accurately mimics the pathological phenotypes of AD remains elusive. In this study, we aimed to induce sporadic AD pathological progression in non-human primates (NHP) through the repeated administration of Aβ oligomers (AβO) via the CBCT-guided intra-cisterna manga (ICM) injection. Cynomolgus monkeys were administered AβO twice a week for four weeks, and then euthanized one week after the final injection. We found that AβO-injected NHP developed AD pathologies, including Aβ deposition, synaptic impairment, and neuroinflammation in the CA1 area of the hippocampus. Additionally, the levels of hyperphosphorylated tau were significantly increased in the cerebrospinal fluid (CSF) of AβO-injected NHP. Our results demonstrate that repeated AβO injection via the ICM route induces several early-stage AD-like neuropathological alterations, including intracellular Aβ accumulation, tau phosphorylation, and synaptic dysfunction. The present study indicates that repeated ICM administration of AβO could be good approach to reproduce a translational NHP model of AD, enabling the study of AD pathogenesis and pre-clinical testing of potential therapeutic candidates for AD.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835759","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}

引用次数: 0

PLGA Nanoparticle-based Anti-TLR2 scFv Gene Delivery for the Treatment of Alzheimer's Disease. 基于PLGA纳米颗粒的抗tlr2 scFv基因递送治疗阿尔茨海默病

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-04-30 Epub Date: 2026-01-19 DOI: 10.5607/en25047

Subeen Lee, Jaesung Lee, Jaekyung Jeon, Hyunji Lee, Boomin Choi, Jinpyo Hong, Sung Joong Lee

{"title":"PLGA Nanoparticle-based Anti-TLR2 scFv Gene Delivery for the Treatment of Alzheimer's Disease.","authors":"Subeen Lee, Jaesung Lee, Jaekyung Jeon, Hyunji Lee, Boomin Choi, Jinpyo Hong, Sung Joong Lee","doi":"10.5607/en25047","DOIUrl":"10.5607/en25047","url":null,"abstract":"In Alzheimer's disease (AD), persistent microglial neuroinflammation and the poor brain exposure and durability of current therapies underscore the need for new, long-acting treatments. We developed a non-viral gene therapy that suppresses microglial Toll-like receptor 2 (TLR2) signaling using poly(lactic-co-glycolic acid) (PLGA) nanoparticles (NPs) loaded with a plasmid encoding the anti-TLR2 single-chain variable fragment (scFv33). Following intra-cisterna magna delivery, PLGA NPs exhibited microglia-biased uptake and enabled brain-wide transgene expression in mice. In 5xFAD mice, a single administration of scFv33 NPs improved recognition memory in the novel object recognition (NOR) assay, outperforming 8 weeks of weekly recombinant scFv33-Fc dosing. Histology showed selective reduction of small hippocampal Aβ plaques and a shift toward a ramified microglial morphology, indicative of reduced activation. In primary neuron-microglia co-culture, scFv33 reduced microglial hypertrophy, restored process complexity, and enhanced Aβ phagocytosis. Together, these data indicate that sustained, local expression of an anti-TLR2 scFv via a clinically translatable PLGA platform recalibrates microglial state and preferentially limits early-stage plaque accumulation, yielding cognitive benefit after a single dose.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":"81-95"},"PeriodicalIF":2.1,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997517","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}

引用次数: 0

The Timing of Attentional Distraction Matters in Facilitating Extinction of Trace Fear Memory. 注意力分散的时机在促进痕量恐惧记忆消退中的作用。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-04-30 Epub Date: 2026-03-11 DOI: 10.5607/en25029

Seung-Min Baek, Sung-Moo Park, Hyoung-Ro Lee, Ung-Gu Kang, Suk-Ho Lee

{"title":"The Timing of Attentional Distraction Matters in Facilitating Extinction of Trace Fear Memory.","authors":"Seung-Min Baek, Sung-Moo Park, Hyoung-Ro Lee, Ung-Gu Kang, Suk-Ho Lee","doi":"10.5607/en25029","DOIUrl":"10.5607/en25029","url":null,"abstract":"Eye movement desensitization and reprocessing (EMDR) is a popular psychotherapy used to alleviate mental distress associated with anxiety and trauma-related disorders. Although working memory taxation has been proposed as an underlying mechanism of the therapy, such claim yet remains controversial due to lack of neurobiological foundations and conflicting findings among studies. In this study, we distracted rats with flickering lights during their training of fear memory extinction. Temporal overlap of twenty-second visual stimulations with the anticipatory shock timing of trace fear conditioning effectively facilitated fear extinction in a subset of animals that showed relatively low freezing during the conditioning day, while random intermittent visual stimulations did not. Moreover, fear extinction in delay fear conditioned animals was not affected either by the same visual stimulations or the stimulations that overlapped with shock timing. These results show that attentional distraction facilitates trace fear extinction, and proper timing is a necessary condition for a sensory stimulation to effectively facilitate trace fear extinction. Implications of our findings in EMDR and potential neurobiological mechanisms are discussed.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":"96-108"},"PeriodicalIF":2.1,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431523","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}

引用次数: 0

AVATAR: AI Vision Analysis for Three-dimensional Action in Real-time. AVATAR：实时三维动作的人工智能视觉分析。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-04-30 Epub Date: 2026-03-03 DOI: 10.5607/en25044

Dae-Gun Kim, Kwanhoo Shin, Anna Shin, Yong-Cheol Jeong, Changbum Ko, Junesu Lee, Seahyung Park, Daesoo Kim

{"title":"AVATAR: AI Vision Analysis for Three-dimensional Action in Real-time.","authors":"Dae-Gun Kim, Kwanhoo Shin, Anna Shin, Yong-Cheol Jeong, Changbum Ko, Junesu Lee, Seahyung Park, Daesoo Kim","doi":"10.5607/en25044","DOIUrl":"10.5607/en25044","url":null,"abstract":"Artificial intelligence (AI) provides new opportunities for high-resolution behavioral analysis and automated, human-free experiments. Here we present AVATAR (AI Vision Analysis for Three-dimensional Action in Real-time). This AI-driven system reconstructs 3D mouse motions by detecting key body parts from synchronized multi-view videos and converting into action skeletons. AVATAR achieves near-human accuracy in pose estimation, enables robust extraction of kinematic and postural features, and supports scalable analysis of model animal behaviors. Using these features represented by 3D action skeleton, LSTM-based model reliably classifies freely moving mouse behaviors during various experimental paradigms with low-latency processing (100 ms) enables real-time closed-loop optogenetic stimulation. As a demonstration of generalizability, we applied AVATAR framework to bottom-view predatory hunting paradigm. AVATARnet accurately detected mouse poses and extracted dynamic behavioral features of the mouse. Using AVATARnet-driven dynamic features, an XGBoost-based classifier automated action segmentation annotation during complex predatory chasing behavior. Together, AVATAR provides 3D pose estimation, dynamic quantification, classification, and closed-loop manipulation in real-time.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":"109-123"},"PeriodicalIF":2.1,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343977","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}

引用次数: 0

Small Molecule Therapeutics Targeting Amyloid-β in Alzheimer's Disease: Mechanisms, Clinical Progress, and Future Strategies. 靶向淀粉样蛋白β治疗阿尔茨海默病的小分子疗法：机制、临床进展和未来策略。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-04-30 Epub Date: 2026-03-30 DOI: 10.5607/en25040

InWook Park, Donghwan Lee, Rachel Sunmin Hong, Hye Yun Kim, YoungSoo Kim

{"title":"Small Molecule Therapeutics Targeting Amyloid-β in Alzheimer's Disease: Mechanisms, Clinical Progress, and Future Strategies.","authors":"InWook Park, Donghwan Lee, Rachel Sunmin Hong, Hye Yun Kim, YoungSoo Kim","doi":"10.5607/en25040","DOIUrl":"10.5607/en25040","url":null,"abstract":"Alzheimer's disease (AD) imposes a growing burden on global healthcare systems. Current therapeutic interventions primarily alleviate cognitive and functional symptoms but have limited impact on the underlying neurodegenerative processes driving disease progression. This underscores the urgent need for treatments that target the pathogenic mechanisms of the disease. Advances in monoclonal antibody therapies against amyloid-β (Aβ) provide encouraging evidence for disease modification, though challenges related to dosing, cost, and safety constrain their broader application. Small molecule therapeutics represent a compelling alternative owing to advantageous properties such as enhanced brain penetration, oral bioavailability, and suitability for long-term administration in elderly patients. Building on these attributes, this review evaluates small molecule therapeutics as promising candidates for AD treatment. It summarizes small molecule compounds targeting Aβ across mechanisms that include modulating production, inhibiting aggregation, disassembling aggregates, enhancing clearance, and mitigating neurotoxicity. A comprehensive assessment of current data emphasizes the importance of continued research to overcome ongoing challenges and fully leverage the potential of small molecules. The limited number of candidates in late-stage clinical trials indicates that substantial efforts are still required to identify and refine effective agents. Continued investigation into their mechanisms and optimization of compound profiles will advance the development of small molecule-based therapies for AD.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":"57-80"},"PeriodicalIF":2.1,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13106959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147572902","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}

引用次数: 0

Blockade of IRE1-XBP1 Signaling Pathway Ameliorates IL-6-dependent Nerve Damage and Neuron Pyroptosis after Subarachnoid Hemorrhage in Mice. 阻断IRE1-XBP1信号通路可改善小鼠蛛网膜下腔出血后il -6依赖性神经损伤和神经元焦亡

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-04-29 DOI: 10.5607/en26003

Huangsuo Wang, Huoquan Tang, Jie Zhou, Bo Li, Xingguang Ren, Yangkai Huang, Zhengkun Liu, Jingjing Hu, Xiaofang Sun, Jian Lu

{"title":"Blockade of IRE1-XBP1 Signaling Pathway Ameliorates IL-6-dependent Nerve Damage and Neuron Pyroptosis after Subarachnoid Hemorrhage in Mice.","authors":"Huangsuo Wang, Huoquan Tang, Jie Zhou, Bo Li, Xingguang Ren, Yangkai Huang, Zhengkun Liu, Jingjing Hu, Xiaofang Sun, Jian Lu","doi":"10.5607/en26003","DOIUrl":"https://doi.org/10.5607/en26003","url":null,"abstract":"Subarachnoid hemorrhage (SAH) often results in severe neurological impairment. While spliced X-box binding protein 1 (XBP1s) has been implicated in brain injury, its specific role and mechanism in SAH-induced mice remain unclear. A murine SAH model was established to explore the function of XBP1 knockdown. Neurological function was evaluated through behavioral tests, brain edema measurement, and hematoxylin and eosin staining. Blood-brain barrier (BBB) integrity and neuronal pyroptosis were assessed using Evans blue extravasation, western blotting, immunofluorescence and LDH release assay. The direct interaction of IL-6 by XBP1s was confirmed using chromatin immunoprecipitation and luciferase reporter assays. Finally, the functional central to our hypothesis was verified by administering exogenous IL-6 or IL-6 blocking antibody to SAH mice. We found that XBP1s and p-IRE1 were significantly up-regulated after SAH. Knockdown of XBP1 ameliorated neurological deficits, preserved BBB integrity (as indicated by increased ZO-1/Occludin and reduced Evans blue leakage), and suppressed neuronal pyroptosis, evidenced by decreased levels of pyroptosis-related proteins and LDH release. Mechanistically, XBP1s was identified as a direct transcriptional enhancer of IL-6. In the mouse SAH model, the protective effects of XBP1 knockdown on the BBB and against pyroptosis were effectively abolished by the exogenous administration of IL-6 and were comparable to administration of the IL-6 blocking antibody. The IRE1-XBP1s signaling axis played an important role in SAH-induced neuronal damage and pyroptosis by directly up-regulating IL-6 expression. Inhibition of this axis represents a mechanistically grounded and promising strategy for SAH intervention.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766602","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}

引用次数: 0

Endogenous Ecotropic Murine Leukemia Virus Promotes Prion Pathogenesis in Senescence-accelerated Mice. 内源性嗜生态小鼠白血病病毒促进衰老加速小鼠的朊病毒发病机制。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-04-29 DOI: 10.5607/en26011

Min-Woo Choi, Mohd Najib Mostafa, Mo-Jong Kim, Byungki Jang, Myung-Ju Choi, Jae-Il Kim, Yong-Sun Kim, Eun-Kyoung Choi

{"title":"Endogenous Ecotropic Murine Leukemia Virus Promotes Prion Pathogenesis in Senescence-accelerated Mice.","authors":"Min-Woo Choi, Mohd Najib Mostafa, Mo-Jong Kim, Byungki Jang, Myung-Ju Choi, Jae-Il Kim, Yong-Sun Kim, Eun-Kyoung Choi","doi":"10.5607/en26011","DOIUrl":"https://doi.org/10.5607/en26011","url":null,"abstract":"Among senescence-accelerated prone mice (SAMP), the SAMP8 and SAMP10 strains exhibit significant age-related deteriorations in learning and memory. Previous studies have reported that SAMP strains carry high level of Akv-type endogenous ecotropic murine leukemia virus (E-MuLV), whereas the senescence-accelerated resistant strain SAMR1 contains very low or undetectable levels of the virus. Retroviral infections, including MuLV, have been implicated in the acceleration of prion pathogenesis. Prion diseases are characterized by neuronal loss, spongiform degeneration, and astrogliosis and are caused by the infectious prion protein (PrPSc), which arises from the misfolding of the normal cellular prion protein (PrPC). Notably SAMP8 mice infected with scrapie exhibit shortened survival and increased PrPSc accumulation compared with SAMR1 mice. In this study, we investigated the role of endogenous E-MuLV to prion disease progression using senescence-accelerated mouse models. Following infection with the 22L scrapie strain, SAMP10 mice displayed significantly shortened survival compared with SAMR1 mice after both intracerebral (IC: 121.8±1.3 vs. 141.0±2.2 days) and intraperitoneal (IP: 184.4±1.3 vs. 216.2±2.7 days) inoculation. SAMP10 mice also showed earlier and more pronounced PrPSc accumulation during the clinical phase, along with enhanced vacuolation. Furthermore, in a cerebellar slice culture model of 22L scrapie infection, treatment with the antiretroviral drug zidovudine significantly reduced PrPSc accumulation in SAMP10 mice. Taken together, these findings suggest that endogenous E-MuLV contribute to the accelerated prion pathogenesis by promoting early and elevated PrPSc accumulation, leading to shortened survival.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147766654","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}

引用次数: 0

Signaling Connectomics: A Brain-wide Framework for Intercellular Communication. 信号连接组学：细胞间通讯的全脑框架。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-04-06 DOI: 10.5607/en26005

Jongpil Shin, Hyeonsik Oh, Yeonji Jeong, Yungyeong Heo, Won Do Heo

{"title":"Signaling Connectomics: A Brain-wide Framework for Intercellular Communication.","authors":"Jongpil Shin, Hyeonsik Oh, Yeonji Jeong, Yungyeong Heo, Won Do Heo","doi":"10.5607/en26005","DOIUrl":"https://doi.org/10.5607/en26005","url":null,"abstract":"Understanding the brain requires mapping not only neuronal circuits but the full landscape of intercellular communication. Here we introduce \"signaling connectomics\", a systems framework for interpreting divergent signaling context. It charts brain-wide signaling across synaptic, neuromodulatory, immune, glial, and vascular pathways. By integrating targeted perturbations with multiplexed molecular and imaging readouts, this approach infers causal signaling networks that operate beyond conventional synapses. It challenges circuit-centric models by emphasizing how dynamic receptor landscapes, extracellular cues, and non-synaptic interactions collectively shape neural function and dysfunction. Combining cell-type-specific optogenetics, biosensors, and spatial transcriptomics, signaling connectomics enables systematic mapping of intercellular signaling dynamics and cross-talk in vivo, providing a multidimensional view of how the brain coordinates activity across diverse cell types. Ultimately, this framework provides conceptual and methodological foundations for linking multicellular signaling to circuit-level plasticity and behavior via explicit causal chains.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622240","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}

引用次数: 0

Neuroprotective and Antidepressant Effects of Tenebrio molitor Larvae Hydrolysate in LPS-induced Neuroinflammation Models. 黄粉虫幼虫水解物对lps诱导的神经炎症模型的神经保护和抗抑郁作用。

IF 2.1 4区医学

Experimental Neurobiology Pub Date : 2026-04-01 DOI: 10.5607/en26002

Younsoo Byun, Jiaxiang Zheng, Yoonhwa Jeong, Jihyun Noh

{"title":"Neuroprotective and Antidepressant Effects of Tenebrio molitor Larvae Hydrolysate in LPS-induced Neuroinflammation Models.","authors":"Younsoo Byun, Jiaxiang Zheng, Yoonhwa Jeong, Jihyun Noh","doi":"10.5607/en26002","DOIUrl":"https://doi.org/10.5607/en26002","url":null,"abstract":"Environmental pollution from synthetic drugs undermines Sustainable Development Goals while exhibiting limited efficacy and adverse effects in mood disorder treatments. Tenebrio molitor larvae (TM) demonstrate significant health benefits including anti-inflammatory, antioxidant, and cognitive enhancing effects. Enzymatic hydrolysis enhances protein bioactivity by improving digestibility and releasing bioactive peptides. This study evaluated neuroprotective effects of TM hydrolysates (TMH) against lipopolysaccharide (LPS)-induced neuroinflammation. Cell viability was measured by WST assay and cytotoxicity was measured by LDH release assay. Inflammatory cytokine mRNA levels were quantified by qRT-PCR, and NF-κB-, MAPKs-, and apoptosis-related biomarkers protein expressions were assessed by western blot. The TMH was administered intracerebroventricularly and LPS was injected intraperitoneally into ICR mice. Behavioral assessments were performed 24 h after LPS injection for sickness-like phenotypes and 28 h after for depressive-like behavior. Mice were sacrificed immediately after the behavior test to collect hippocampal tissue for cytokine mRNA analyses. TMH prevented LPS-induced sickness-like phenotypes and depressive-like behavior increases. Hippocampal IL-1β mRNA levels decreased significantly while IL-6, TNF-α, and IL-10 expression showed downward trends. Cell viability was preserved with reduced LDH release and attenuated upregulation of IL-1β, NF-κB, JNK, ERK, and Caspase-3 in PC-12 cells. TMH demonstrated robust protection against LPS-induced neuroinflammatory and behavioral alterations, indicating therapeutic potential for mood disorder interventions through sustainable, bioactive compound utilization. TMH mitigates both neurotoxic and depressive-like effects of systemic LPS in complementary cell and animal models, supporting its potential development as an eco-friendly, non-synthetic therapeutic agent for neuroinflammatory mood disorders.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590934","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}

引用次数: 0