Hao Peng, Qianqian Ge, Tianshuai Xu, Yifang He, Long Xu, Yi Yang, Sijin Wu, Jianghong He, Juanning Si
{"title":"Repetitive transcranial magnetic stimulation frequency influences the hemodynamic responses in patients with disorders of consciousness.","authors":"Hao Peng, Qianqian Ge, Tianshuai Xu, Yifang He, Long Xu, Yi Yang, Sijin Wu, Jianghong He, Juanning Si","doi":"10.1016/j.neures.2025.02.003","DOIUrl":"10.1016/j.neures.2025.02.003","url":null,"abstract":"<p><p>Repetitive transcranial magnetic stimulation (rTMS) emerges as a promising non-invasive neuromodulation technique for the treatment of patients with disorders of consciousness (DOC). The selection of rTMS parameters significantly influences the clinical therapeutic effects. However, the differences in spatiotemporal responsiveness of the brain under different rTMS stimulation frequencies remain unclear. In this pilot study, functional near-infrared spectroscopy (fNIRS) was used to evaluate the spatiotemporal differences in hemodynamic responses elicited by rTMS at different frequencies (1, 5, 10, 15, and 20 Hz) over left dorsolateral prefrontal cortex (F3). The results showed that the distribution patterns of the rTMS-evoked hemodynamic responses varied across different frequencies, indicating that rTMS frequency influences the hemodynamic responses in patients with DOC. Specifically, 10 Hz rTMS evoked strong positive hemodynamic responses over the frontal cortex, particularly in the right dorsolateral prefrontal cortex (R-DLPFC). Additionally, 20 Hz rTMS produced largepositive hemodynamic responses over the motor-related cortex, especially the right premotor cortex (R-PreM) and right primary sensorimotor cortex (PSMC). The current findings suggested that fNIRS can be used as a promising tool for evaluating the effects of rTMS in patients with DOC. Moreover, it provides useful guidance for the personalized design of rTMS parameters in a clinical environment.</p>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374324","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":"Siponimod inhibits microglial inflammasome activation.","authors":"Hiroyasu Komiya, Hideyuki Takeuchi, Akihiro Ogasawara, Yuki Ogawa, Shun Kubota, Shunta Hashiguchi, Keita Takahashi, Misako Kunii, Kenichi Tanaka, Mikiko Tada, Hiroshi Doi, Fumiaki Tanaka","doi":"10.1016/j.neures.2025.02.002","DOIUrl":"10.1016/j.neures.2025.02.002","url":null,"abstract":"<p><p>Siponimod is the first oral drug approved for active secondary progressive multiple sclerosis. It acts as a functional antagonist of sphingosine-1-phosphate (S1P) receptor 1 (S1P<sub>1</sub>) through S1P<sub>1</sub> internalization, and also serves an agonist of S1P<sub>5</sub>; however, the detailed mechanisms of its therapeutic effects on glial cells have yet to be elucidated. In this study, we investigated the anti-inflammatory mechanism of siponimod in microglia. Pretreatment with either siponimod or the S1P<sub>1</sub> antagonist W146 significantly suppressed the production of interleukin-1β in activated microglia stimulated with lipopolysaccharide plus nigericin, an inflammasome activator. Furthermore, siponimod treatment reduced the protein levels of cleaved caspase-1 and inhibited the formation of aggregates of apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC specks) in microglia. Our data indicate that siponimod achieves its anti-inflammatory effects by inhibiting inflammasome activation in microglia via S1P<sub>1</sub> antagonism. This process is inferred to play a crucial role in mitigating the secondary progression of multiple sclerosis, where microglial activation in the gray matter is considered a key pathological factor.</p>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374235","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}
Wajd Amly, Chih-Yang Chen, Hirotaka Onoe, Tadashi Isa
{"title":"Different properties of successful and error saccades in marmosets.","authors":"Wajd Amly, Chih-Yang Chen, Hirotaka Onoe, Tadashi Isa","doi":"10.1016/j.neures.2025.02.001","DOIUrl":"10.1016/j.neures.2025.02.001","url":null,"abstract":"<p><p>Various oculomotor tasks have been used to study eye movements, cognitive control, attention, and neurological disorders. Typically, analysis focuses on successful trials, where the saccade lands very close to the intended target, in both humans or non-human primates (NHPs). Error trials, in which the saccade fails to land on the intended target, are often excluded from these analyses. In this study, we hypothesized that saccades contain information that can predict whether they will result in success or not. We collected data from common marmosets performing the gap saccade task and the oculomotor delayed response task. Successful saccades in both tasks were characterized by higher peak velocities, shorter durations, and shorter latencies compared to errant saccades, regardless of whether the amplitudes were matched or not. These results were further validated using a generalized linear model, with saccade velocity, duration, and latency as predictors. The model demonstrated high accuracy in distinguishing between behavioural outcomes. Our findings suggest that the likelihood of a saccadic eye movement leading to a successful outcome may be predetermined, potentially reflecting the interaction between cognitive processes and saccade programming.</p>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374323","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":"Memory-related neurophysiological mechanisms in the hippocampus underlying stress susceptibility","authors":"Nahoko Kuga, Takuya Sasaki","doi":"10.1016/j.neures.2022.07.010","DOIUrl":"10.1016/j.neures.2022.07.010","url":null,"abstract":"<div><div>Stress-induced psychiatric symptoms, such as increased anxiety, decreased sociality, and depression, differ considerably across individuals. The cognitive model of depression proposes that biased negative memory is a crucial determinant in the development of mental stress-induced disorders. Accumulating evidence from both clinical and animal studies has demonstrated that such biased memory processing could be triggered by the hippocampus, a region well known to be involved in declarative memories. This review mainly describes how memory-related neurophysiological mechanisms in the hippocampus and their interactions with other related brain regions are involved in the regulation of stress susceptibility and discusses potential interventions to prevent and treat stress-related psychiatric symptoms. Further neurophysiological insights based on memory mechanisms are expected to devise personalized prevention and therapy to confer stress resilience.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"211 ","pages":"Pages 3-9"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40587273","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}
{"title":"Bidirectional relationship between sleep and depression","authors":"Shinnosuke Yasugaki , Hibiki Okamura , Ami Kaneko , Yu Hayashi","doi":"10.1016/j.neures.2023.04.006","DOIUrl":"10.1016/j.neures.2023.04.006","url":null,"abstract":"<div><div>Patients with depression almost inevitably exhibit abnormalities in sleep, such as shortened latency to enter rapid eye movement (REM) sleep and decrease in electroencephalogram delta power during non-REM sleep. Insufficient sleep can be stressful, and the accumulation of stress leads to the deterioration of mental health and contributes to the development of psychiatric disorders. Thus, it is likely that depression and sleep are bidirectionally related, i.e. development of depression contributes to sleep disturbances and vice versa. However, the relation between depression and sleep seems complicated. For example, acute sleep deprivation can paradoxically improve depressive symptoms. Thus, it is difficult to conclude whether sleep has beneficial or harmful effects in patients with depression. How antidepressants affect sleep in patients with depression might provide clues to understanding the effects of sleep, but caution is required considering that antidepressants have diverse effects other than sleep. Recent animal studies support the bidirectional relation between depression and sleep, and animal models of depression are expected to be beneficial for the identification of neuronal circuits that connect stress, sleep, and depression. This review provides a comprehensive overview regarding the current knowledge of the relationship between depression and sleep.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"211 ","pages":"Pages 57-64"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9414711","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}
{"title":"Regulation of adult-born and mature neurons in stress response and antidepressant action in the dentate gyrus of the hippocampus","authors":"Eri Segi-Nishida, Kanzo Suzuki","doi":"10.1016/j.neures.2022.08.010","DOIUrl":"10.1016/j.neures.2022.08.010","url":null,"abstract":"<div><div>The dentate gyrus (DG) of the hippocampus has been implicated in the regulation of stress responses, and in the pathophysiology and treatment of depression. This review discusses the cellular changes caused by chronic stress and the cellular role of the DG in stress-induced behavioral changes and its antidepressant-like effects. Regarding adult-born neurogenic processes in the DG, chronic stress, such as repeated social defeat, suppresses cell proliferation during and immediately after stress; however, this effect is transient. The subsequent differentiation and survival processes are differentially regulated depending on the timing and sensitivity of stress. The activation of young adult-born neurons during stress contributes to stress resilience, while the transient increase in the survival of adult-born neurons after the cessation of stress seems to promote stress susceptibility. In mature granule neurons, the predominant cells in the DG, synaptic plasticity is suppressed by chronic stress. However, a group of mature granule neurons is activated by chronic stress. Chronic antidepressant treatment can transform mature granule neurons to a phenotype resembling that of immature neurons, characterized as “dematuration”. Adult-born neurons suppress the activation of mature granule neurons during stress, indicating that local neural interactions within the DG are important for the stress response. Elucidating the stress-associated context- and timing-dependent cellular changes and functions in the DG will provide insights into stress-related psychiatric diseases.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"211 ","pages":"Pages 10-15"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40448045","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}
Lyonna F. Parise, C. Joseph Burnett, Scott J. Russo
{"title":"Early life stress and altered social behaviors: A perspective across species","authors":"Lyonna F. Parise, C. Joseph Burnett, Scott J. Russo","doi":"10.1016/j.neures.2023.11.005","DOIUrl":"10.1016/j.neures.2023.11.005","url":null,"abstract":"<div><div>Childhood and adolescent affiliations guide how individuals engage in social relationships throughout their lifetime and adverse experiences can promote biological alterations that facilitate behavioral maladaptation. Indeed, childhood victims of abuse are more likely to be diagnosed with conduct or mood disorders which are both characterized by altered social engagement. A key domain particularly deserving of attention is aggressive behavior, a hallmark of many disorders characterized by deficits in reward processing. Animal models have been integral in identifying both the short- and long-term consequences of stress exposure and suggest that whether it is disruption to parental care or social isolation, chronic exposure to early life stress increases corticosterone, changes the expression of neurotransmitters and neuromodulators, and facilitates structural alterations to the hypothalamus, hippocampus, and amygdala, influencing how these brain regions communicate with other reward-related substrates. Herein, we describe how adverse early life experiences influence social behavioral outcomes across a wide range of species and highlight the long-term biological mechanisms that are most relevant to maladaptive aggressive behavior.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"211 ","pages":"Pages 65-74"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11102940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138295629","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}
Benjamin M. Siemsen, Daniela Franco, Mary Kay Lobo
{"title":"Corticostriatal contributions to dysregulated motivated behaviors in stress, depression, and substance use disorders","authors":"Benjamin M. Siemsen, Daniela Franco, Mary Kay Lobo","doi":"10.1016/j.neures.2022.12.014","DOIUrl":"10.1016/j.neures.2022.12.014","url":null,"abstract":"<div><div>Coordinated network activity, particularly in circuits arising from the prefrontal cortex innervating the ventral striatum, is crucial for normal processing of reward-related information which is perturbed in several psychiatric disorders characterized by dysregulated reward-related behaviors. Stress-induced depression and substance use disorders (SUDs) both share this common underlying pathology, manifested as deficits in perceived reward in depression, and increased attribution of positive valence to drug-predictive stimuli and dysfunctional cognition in SUDs. Here we review preclinical and clinical data that support dysregulation of motivated and reward-related behaviors as a core phenotype shared between these two disorders. We posit that altered processing of reward-related stimuli arises from dysregulated control of subcortical circuits by upstream regions implicated in executive control. Although multiple circuits are directly involved in reward processing, here we focus specifically on the role of corticostriatal circuit dysregulation. Moreover, we highlight the growing body of evidence indicating that such abnormalities may be due to heightened neuroimmune signaling by microglia, and that targeting the neuroimmune system may be a viable approach to treating this shared symptom.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"211 ","pages":"Pages 37-48"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10550554","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}
{"title":"Resolution of depression: Antidepressant actions of resolvins","authors":"Satoshi Deyama , Katsuyuki Kaneda , Masabumi Minami","doi":"10.1016/j.neures.2022.10.006","DOIUrl":"10.1016/j.neures.2022.10.006","url":null,"abstract":"<div><div>Major depressive disorder, one of the most widespread mental illnesses, brings about enormous individual and socioeconomic consequences. Conventional monoaminergic antidepressants require weeks to months to produce a therapeutic response, and approximately one-third of the patients fail to respond to these drugs and are considered treatment-resistant. Although recent studies have demonstrated that ketamine, an <em>N</em>-methyl-<span>D</span>-aspartate receptor antagonist, produces rapid antidepressant effects in treatment-resistant patients, it also has undesirable side effects. Hence, rapid-acting antidepressants that have fewer adverse effects than ketamine are urgently required. <span>D</span>-series (RvD1–RvD6) and E-series (RvE1–RvE4) resolvins are endogenous lipid mediators derived from docosahexaenoic and eicosapentaenoic acids, respectively. These mediators reportedly play a pivotal role in the resolution of acute inflammation. In this review, we reveal that intracranial infusions of RvD1, RvD2, RvE1, RvE2, and RvE3 produce antidepressant-like effects in various rodent models of depression. Moreover, the behavioral effects of RvD1, RvD2, and RvE1 are mediated by the activation of the mechanistic target of rapamycin complex 1, which is essential for the antidepressant-like actions of ketamine. Finally, we briefly provide our perspective on the possible role of endogenous resolvins in stress resilience.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"211 ","pages":"Pages 85-92"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40579373","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}
{"title":"Synaptic plasticity in fronto-insular circuits underlying stress susceptibility and resilience","authors":"Devin Rocks, Conor Liston","doi":"10.1016/j.neures.2024.12.006","DOIUrl":"10.1016/j.neures.2024.12.006","url":null,"abstract":"<div><div>Chronic stress may trigger depressive episodes in vulnerable individuals but the underlying mechanisms remain incompletely understood. Converging lines of evidence indicate that these mechanisms may converge on the dysregulation of synaptic transmission in the anterior cingulate and anterior insula, disrupting motivation and hedonic function. In this review, we examine how chronic stress and antidepressants modulate synaptic connectivity in stress-sensitive brain circuits. We discuss the roles of various synaptic and molecular pathways in these processes, their interaction with circadian rhythms, and their contributions to the regulation of mood, with a particular focus on anhedonia. In the short term, stress effects on neuronal activity may be adaptive, but repeated engagement of these adaptations may lead to circuit dysfunction—a phenomenon known as allostatic load. We also highlight new insights from neuroimaging studies that suggest that synaptic reorganization within fronto-insular circuits that process valence, salience, and motivation could play a critical role in driving risk for depression and transitioning between mood states. We propose a working model in which synapse loss in the anterior cingulate and anterior insula may contribute to depression by disrupting effort valuation computations, which regulate decision making and hedonic function by integrating information about anticipated rewards and the effort required to obtain them.</div></div>","PeriodicalId":19146,"journal":{"name":"Neuroscience Research","volume":"211 ","pages":"Pages 24-36"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143167881","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}