Neuroscience ResearchPub Date : 2026-01-01Epub Date: 2025-12-03DOI: 10.1016/j.neures.2025.105004
Mao Otake , Takuya Ibaraki , Ming Chang , Masaki Iwasaki , Go Taniguchi , Toshitaka Yamakawa , Shunsuke Takagi , Takashi Takeuchi , Hidehiko Takahashi , Miho Miyajima
{"title":"Performance evaluation of the earphone-type electroencephalogram for alpha wave detection","authors":"Mao Otake , Takuya Ibaraki , Ming Chang , Masaki Iwasaki , Go Taniguchi , Toshitaka Yamakawa , Shunsuke Takagi , Takashi Takeuchi , Hidehiko Takahashi , Miho Miyajima","doi":"10.1016/j.neures.2025.105004","DOIUrl":"10.1016/j.neures.2025.105004","url":null,"abstract":"<div><div>Electroencephalography (EEG) is useful for monitoring brain functions. Recently, wearable earphone-type EEG devices that can be easily used at home have emerged. Although their application scope is expanding, their comfort and detection validity have yet to be sufficiently validated. Herein, we examined the capability of an earphone-type EEG device to record EEG phenomena and compared with conventional scalp EEG. Simultaneous scalp and earphone-type EEG measurements were performed for 30 min, including eyes-open /eye-closed and sleeping tasks, on 25 healthy participants. We compared the detection validity of alpha waves using power spectrum analysis and statistical procedures. Among the 25 participants, 11 participants with available sleep EEG data were included in the final analysis. Compared with the eyes-closed, a reduction in alpha power was observed under the eyes-open condition in the alpha frequency band (8–13 Hz). Similarly, most participants exhibited decreased alpha power during sleep compared with wakefulness. These results indicate that the earphone-type EEG systems record canonical brainwaves in healthy individuals.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"222 ","pages":"Article 105004"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145682346","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":"Acute stress suppresses hunger-driven food seeking through PVN activation: Reversal by anxiolytic drug and ghrelin receptor agonist, with anxiolytic-like effects of refeeding","authors":"Ryusei Tojo , Mayuka Tashiro , Haruka Takahashi , Hideki Tamura","doi":"10.1016/j.neures.2025.104989","DOIUrl":"10.1016/j.neures.2025.104989","url":null,"abstract":"<div><div>Feeding behavior is influenced by both metabolic drive and emotional context, yet how acute stress interferes with hunger-driven motivation remains poorly understood. Using a conflict-based open-field feeding paradigm, we examined how 30-min restraint stress alters food-seeking behavior in fasted mice and how pharmacological or physiological interventions modulate this effect. Acute restraint abolished fasting-induced increases in food seeking and intake, an effect that was reversed by intraperitoneal diazepam, an anxiolytic, and by MK-677, a ghrelin receptor agonist that enhances appetite. To identify neural correlates, we quantified c-Fos (neuronal activation) and phosphorylated pyruvate dehydrogenase (pPDH; neuronal inhibition) in the paraventricular hypothalamic nucleus (PVN). Diazepam suppressed restraint-induced c-Fos expression, whereas MK-677 increased pPDH, revealing distinct PVN signatures for anxiolysis and enhanced feeding drive. Notably, refeeding after fasting induced a similar pPDH-dominant pattern and attenuated stress-induced anxiety-related behaviors, indicating that restoration of energy balance exerts intrinsic anti-stress effects through PVN inhibition. Together, these findings reveal that acute stress suppresses hunger-driven food seeking via PVN activation, pharmacological inhibition reverses this suppression, and physiological refeeding promotes stress resilience via PVN-medicated inhibition, highlighting PVN modulation as a shared mechanism linking emotional and metabolic homeostasis.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"222 ","pages":"Article 104989"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145557556","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}
Neuroscience ResearchPub Date : 2026-01-01Epub Date: 2025-11-28DOI: 10.1016/j.neures.2025.104993
Keita Matsumoto, Sumihiro Maeda
{"title":"The application of directly induced neurons into neurodegenerative disease modeling","authors":"Keita Matsumoto, Sumihiro Maeda","doi":"10.1016/j.neures.2025.104993","DOIUrl":"10.1016/j.neures.2025.104993","url":null,"abstract":"<div><div>The advent of directly induced neurons (iNs) from human somatic cells has revolutionized disease modeling in neurodegeneration. This approach bypasses pluripotent stage during the neuronal cell inducing steps and preserves donor age-related signatures. This review explores the trajectory of iNs, including multiple induction methods, their applications in modeling neurodegenerative diseases, recent innovations such as three-dimensional (3D) culture platforms, and their potential to advance personalized medicine.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"222 ","pages":"Article 104993"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145648999","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}
Neuroscience ResearchPub Date : 2026-01-01Epub Date: 2025-12-03DOI: 10.1016/j.neures.2025.105005
Kumi O. Kuroda, Kazunari Miyamichi
{"title":"Neuroscience Research Special Issue","authors":"Kumi O. Kuroda, Kazunari Miyamichi","doi":"10.1016/j.neures.2025.105005","DOIUrl":"10.1016/j.neures.2025.105005","url":null,"abstract":"","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"222 ","pages":"Article 105005"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145687740","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":"The TDP-43I383V heterozygous mutation results in increased TDP-43 expression and altered neuronal activity in ALS patient-derived iPSC motor neurons","authors":"Ryo Chikuchi , Yuta Kato , Aya Tomatsu , Shuto Nishisaki , Yu Kawakami , Takashi Yoshimura , Jiayi Li , Yohei Iguchi , Kazunari Onodera , Rina Hashimoto , Ikuko Aiba , Ryoichi Nakamura , Genki Tohnai , Naoki Atsuta , Gen Sobue , Yohei Okada , Masahisa Katsuno , Satoshi Yokoi","doi":"10.1016/j.neures.2025.105003","DOIUrl":"10.1016/j.neures.2025.105003","url":null,"abstract":"<div><div>TAR-binding protein 43 (TDP-43) is a pathogenic RNA-binding protein associated with amyotrophic lateral sclerosis (ALS). To elucidate the pathogenesis of ALS, we generated induced pluripotent stem cells (iPSCs) from lymphoblastoid cell line (LCL) cells of an ALS patient with the TDP-43<sup>I383V</sup> heterozygous mutation. Furthermore, we generated isogenic wild-type iPSCs from wild-type LCL cells using scarless genome editing with CRISPR/Cas9. A modified iPSC-derived motor neuron culture method utilizing BrainPhys neuronal medium and rat astrocyte co-culture effectively promoted and maintained neuronal activity. Under these conditions, the TDP-43<sup>I383V</sup> heterozygous mutation resulted in increased TDP-43 protein expression through prolonged stabilization. Moreover, mutant iPSC-derived motor neurons showed increased numbers of pre-synapses and altered neuronal activity. These results suggest that the modified motor neuron culture method can help elucidate abnormalities in TDP-43 expression, synapse formation, and neuronal activity caused by the heterozygous TDP-43<sup>I383V</sup> mutation. The model developed in this study has the potential to facilitate the analysis of the early pathological phenotype of ALS.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"222 ","pages":"Article 105003"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145695898","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":"A computational model of canonical cortical microcircuits for dynamic Bayesian inference and control as inference","authors":"Naohiro Yamauchi , Yoshimasa Tawatsuji , Yudai Suzuki , Hiroshi Yamakawa , Kenji Doya","doi":"10.1016/j.neures.2025.105002","DOIUrl":"10.1016/j.neures.2025.105002","url":null,"abstract":"<div><div>Canonical cortical microcircuits (CCMs), a six-layer architecture conserved across the mammalian neocortex, play a crucial role in cognitive functions such as sensory inference, decision-making, and motor planning. However, the computational mechanisms underlying these functions remain unclear, and existing models often lack detailed representations of cell types and interlayer connectivity. In this study, we applied the structure-constrained interface decomposition (SCID) method (Yamakawa, 2021) to construct a biologically plausible computational model of CCMs for dynamic Bayesian inference (DBI) and control as inference (CAI). Our model explicitly assigns computational roles to all major excitatory neuronal populations and incorporates the contributions of inhibitory neurons via circuit motifs. Based on this framework, we constructed CCM models of the somatosensory cortex for DBI and motor cortex for CAI. Through simulations of a mouse lever-push/pull perceptual decision-making and control task, our model reproduced key behavioral features, including psychometric curves and “change of mind” behaviors. Furthermore, we conducted layer-specific perturbation simulations that produced experimentally testable predictions about the functional roles of different cortical layers. Based on the duality of inference and control, this study addresses the long-standing challenge of giving a unified account of CCMs’ functions in sensory and motor cortices.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"222 ","pages":"Article 105002"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145695880","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":"Graded regulation of microtubule-binding of Tau by the phosphorylation state of the proline-rich region in living neurons","authors":"Rinaho Nakata , Tomohiro Torii , Tomohiro Miyasaka , Hiroaki Misonou","doi":"10.1016/j.neures.2025.104987","DOIUrl":"10.1016/j.neures.2025.104987","url":null,"abstract":"<div><div>Tau protein is a microtubule-associated protein that plays a crucial role in maintaining neuronal morphology and axonal transport. While phosphorylation is known to regulate Tau-microtubule interactions, the contribution of specific phosphorylation patterns <em>in situ</em> remains poorly understood due to the complexity of the intracellular environment. In this study, we combined fluorescence recovery after photobleaching (FRAP) in primary cultured rat hippocampal neurons with dephosphorylation-mimetic mutations and computational modeling to analyze the effects of phosphorylation on Tau-microtubule interaction. We particularly focused on the proline-rich region, of which phosphorylation has been studied in physiological and pathological perspectives, and generated a dephosphorylation-mimetic Tau mutant by substituting key phosphorylation sites with alanine residues and compared its microtubule-binding dynamics to those of WT-Tau in FRAP experiments. Experimental data, together with simulation-based parameter exploration, revealed that the overall number of non-phosphorylated sites plays a more dominant role than their specific locations in modulating Tau-microtubule affinity. These findings provide new insights into the post-translational regulation of Tau and establish a computational-experimental framework for interrogating intracellular protein dynamics.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"222 ","pages":"Article 104987"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145564633","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}
Neuroscience ResearchPub Date : 2025-12-01Epub Date: 2025-11-11DOI: 10.1016/j.neures.2025.104986
Takahiro Morito , Naoto Watamura
{"title":"Experimental modeling for tauopathies: An isogenic panel of humanized MAPT knock-in mice","authors":"Takahiro Morito , Naoto Watamura","doi":"10.1016/j.neures.2025.104986","DOIUrl":"10.1016/j.neures.2025.104986","url":null,"abstract":"<div><div>Tauopathies are a group of neurodegenerative diseases characterized by the aberrant accumulation of tau protein in the brain. While numerous mouse models have been developed to study tauopathies, the majority depend on tau overexpression, which may encompass non-physiological artifacts and limit the translational relevance of findings. In this review, we highlight the development and application of an isogenic panel of <em>MAPT</em> knock-in (KI) mouse lines that carry single or multiple pathogenic mutations within the human <em>MAPT</em> gene. In these models, the endogenous murine <em>Mapt</em> gene was replaced with the humanized <em>MAPT</em> sequence, and tau is expressed under the control of the native murine <em>Mapt</em> promoter. This approach preserves spatiotemporal regulation of tau, providing a more physiological representation of human tauopathies. As such, these mutant <em>MAPT</em> KI models serve as powerful tools for elucidating the pathomechanisms of tauopathies and discovering drugs that aid tau-mediated neurodegeneration.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"221 ","pages":"Article 104986"},"PeriodicalIF":2.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145513472","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}
Neuroscience ResearchPub Date : 2025-12-01Epub Date: 2025-10-25DOI: 10.1016/j.neures.2025.104972
Ryo Ito , Satoko Amemori , Ken-ichi Amemori
{"title":"Predictive coding in the primate brain: From visual to fronto-limbic systems","authors":"Ryo Ito , Satoko Amemori , Ken-ichi Amemori","doi":"10.1016/j.neures.2025.104972","DOIUrl":"10.1016/j.neures.2025.104972","url":null,"abstract":"<div><div>Predictive coding theory has emerged as a powerful framework for understanding neural information processing, offering a unified account of perception, cognition, and behavior through hierarchical minimization of prediction error. Notably, recent studies emphasize that the anatomical hierarchy and neurophysiological dynamics of the primate visual cortex are closely aligned with this framework. In this review, we examine the neural implementation of hierarchical information processing in the primate cerebral cortex from multiple perspectives, focusing on predictive coding theory. We aim to integrate findings from mathematical modeling, cortical microcircuits, laminar structure, neural oscillations, and clinical research. One of the central themes emerging from this integrative perspective is that interareal communication in the cortex is characterized by frequency-specific neural dynamics. Beta-band oscillations support top-down signals, whereas gamma-band oscillations convey bottom-up signals. These patterns closely reflect the directionality of anatomically defined projections. We also highlight that neural networks trained to predict upcoming visual input can develop functional properties observed in the primate visual system without these properties being explicitly supervised. Finally, we argue that hierarchical interaction provides a valuable perspective for understanding large-scale network dysfunctions associated with disorders such as depression and anxiety. These abnormalities may reflect disruptions in predictive signaling across functional domains rather than isolated regional deficits.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"221 ","pages":"Article 104972"},"PeriodicalIF":2.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145419993","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}
Neuroscience ResearchPub Date : 2025-12-01Epub Date: 2025-11-08DOI: 10.1016/j.neures.2025.104982
Jingyi Xie , Xiaotong Zhang , Shengli Li , Zichen Chen , Xujia Zhang , Jinyi Tian , Yulu Yan , Yongqi Pan , Ke Shi , Jianbin Sun , Teru Kamogashira , Ying Gao
{"title":"A mouse model of bilateral acute inner-ear (labyrinthine) injury with vestibular involvement reveals functional, behavioral, and histological correlates of vestibular compensation","authors":"Jingyi Xie , Xiaotong Zhang , Shengli Li , Zichen Chen , Xujia Zhang , Jinyi Tian , Yulu Yan , Yongqi Pan , Ke Shi , Jianbin Sun , Teru Kamogashira , Ying Gao","doi":"10.1016/j.neures.2025.104982","DOIUrl":"10.1016/j.neures.2025.104982","url":null,"abstract":"<div><div>Bilateral vestibular dysfunction disrupts balance and spatial orientation, yet mechanisms of injury and compensation remain incompletely defined. We established a mouse model of bilateral acute inner-ear (labyrinthine) injury with vestibular involvement by sequentially incising the round and oval windows, and evaluate auditory brainstem responses (ABR), vestibular sensory-evoked potentials (VsEP), behavior, and histology across postoperative days 1–28. Threshold elevations and behavioral impairment peaked on day 3, with hair-cell degeneration most prominent early and partial morphological recovery by day 28. These findings delineate the acute injury phase and early stabilization, providing a platform to study vestibular repair and functional recovery.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"221 ","pages":"Article 104982"},"PeriodicalIF":2.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145489232","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}