Neuroscience Letters最新文献_第2页

Mitochondrial dysfunction and aging can be alleviated by modulating calcineurin and cardiolipin dynamics following stroke 脑卒中后可通过调节钙调磷酸酶和心磷脂动态来缓解线粒体功能障碍和衰老。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-10-06 DOI: 10.1016/j.neulet.2025.138410

Pallab Bhattacharya , Shailendra Saraf , Anirban Barik , Bijoyani Ghosh , Aishika Datta , Davendra Singh Malik

{"title":"Mitochondrial dysfunction and aging can be alleviated by modulating calcineurin and cardiolipin dynamics following stroke","authors":"Pallab Bhattacharya , Shailendra Saraf , Anirban Barik , Bijoyani Ghosh , Aishika Datta , Davendra Singh Malik","doi":"10.1016/j.neulet.2025.138410","DOIUrl":"10.1016/j.neulet.2025.138410","url":null,"abstract":"<div><div>The crucial influence of mitochondria in ischemic stroke pathophysiology presents many unexplored yet promising avenues for therapeutic strategies and clinical outcomes. Post-stroke mitochondrial dysfunction contributes to aggravated levels of calcium overload and apoptosis. This dysfunction is signified by disruption of the mitochondrial lipids such as cardiolipin, along with mitochondrial DNA mutation, leading to an imbalance in mitophagy. Calcium overload-mediated calcineurin overexpression has been reported to exacerbate mitochondrial damage and further contribute to neuronal apoptosis. In our study, we explored the alterations in the mitochondrial function following inhibition of the calcium-mediated calcineurin levels in post-stroke condition. In a rodent model of middle cerebral artery occlusion (MCAo), we observed that the inhibition of the calcium channels in post-stroke condition led to restored neuronal histology and viability following upregulation of the antioxidant levels. At the mitochondrial level, calcium channel inhibition downregulated calcineurin activation and normalized cardiolipin concentration, mitochondrial membrane potential, and respiratory control ratio in post-stroke condition. This inhibition also balanced the mitochondrial dynamics proteins and mitophagy towards neuronal recovery following ischemic stress. Moreover, it also normalized the expression of TERT, a key marker of mitochondrial health and aging. These findings highlight the role of calcium-mediated calcineurin in influencing mitochondrial dysfunction and aging in ischemic stroke. Thus, calcium channel inhibition offers a promising therapeutic strategy by preserving mitochondrial integrity and promoting neuroprotection following stroke.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"868 ","pages":"Article 138410"},"PeriodicalIF":2.0,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145252190","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

Regional differences in oxytocin and vasopressin 1a receptor functionality in mouse embryonic brain development 小鼠胚胎脑发育中催产素和抗利尿激素1a受体功能的区域差异。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-10-05 DOI: 10.1016/j.neulet.2025.138409

Elliot Sommer , Heather K. Caldwell

{"title":"Regional differences in oxytocin and vasopressin 1a receptor functionality in mouse embryonic brain development","authors":"Elliot Sommer , Heather K. Caldwell","doi":"10.1016/j.neulet.2025.138409","DOIUrl":"10.1016/j.neulet.2025.138409","url":null,"abstract":"<div><div>There is mounting evidence that the oxytocin (Oxt) and vasopressin (Avp) systems contribute to early brain development. Work from transgenic mouse models as well as pharmacological manipulation of the Oxt and Avp systems suggests that signaling through the Oxt receptor (Oxtr) and the Avp 1a receptor (Avpr1a) during embryonic brain development affects behavior in adulthood. Unfortunately, at this time, very little is known or understood about where in the brain Oxtr and Avpr1a occurs during embryonic development or what the downstream consequences may be. To help provide some answers, Oxtr- and Avpr1a-stimulated G-protein coupled receptor binding assays were performed using guanosine 5′-(γ-thio)triphosphate, a non-hydrolyzable analog of guanosine triphosphate, to determine the functionality of the Oxtr and Avpr1a in both sexes at embryonic day (E) 14.5, E16.5, and E18.5. Based on previous work, we hypothesized that the Oxtr and Avpr1a would be functional in both sexes by E16.5 and activated by Oxt and Avp, respectively. The data suggest that while the Oxtr and Avpr1a are functional in both sexes starting at E16.5, where in the brain they are functional is not fully aligned with where there is known receptor binding. For the Oxtr, at E16.5, functional binding was observed in the ventricular and subventricular zones of the cortical and septal neuroepithelium and the amygdalar area, this shifted by E18.5 with functional binding observed only in the ventricular and subventricular septal neuroepithelium and the amygdalar area, with no functional binding observed in the ventricular and subventricular cortical neuroepithelium. For the Avpr1a, at E16.5, functional binding was only observed in the ventral hypothalamic area but by E18.5 functional binding was observed across numerous brain regions. Taken together, these data suggest that Oxtr and Avpr1a signaling is positioned to have site-specific effects on mouse brain development starting at E16.5.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"868 ","pages":"Article 138409"},"PeriodicalIF":2.0,"publicationDate":"2025-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244732","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

Increased reactive oxygen species in the spinal cord drive renal sympathetic vasomotor activity in Goldblatt hypertensive rats Goldblatt高血压大鼠脊髓活性氧增加驱动肾交感血管舒张活性。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-10-03 DOI: 10.1016/j.neulet.2025.138408

Fernanda M. Tagliapietra, Maycon I.O. Milanez, Edina da Luz Abreu, Erika E. Nishi, Cássia T. Bergamaschi, Ruy R. Campos

{"title":"Increased reactive oxygen species in the spinal cord drive renal sympathetic vasomotor activity in Goldblatt hypertensive rats","authors":"Fernanda M. Tagliapietra, Maycon I.O. Milanez, Edina da Luz Abreu, Erika E. Nishi, Cássia T. Bergamaschi, Ruy R. Campos","doi":"10.1016/j.neulet.2025.138408","DOIUrl":"10.1016/j.neulet.2025.138408","url":null,"abstract":"<div><div>Increased production of reactive oxygen species (ROS) in brain regions contributes to the sympathetic vasomotor overactivity in Goldblatt hypertension (2K1C). Previously, studies reported that overexpression of spinal angiotensin II (Ang II) type I (AT1) contributes to sympathetic vasomotor overactivation in 2K1C rats. Considering that Ang II leads to an imbalance of oxidative stress, the present study evaluated the role of spinal ROS in regulating the activity of sympathetic preganglionic neurons in 2K1C rats. Hypertension was induced by clipping the left renal artery. Six weeks after clipping, a catheter was inserted into the subarachnoid space and advanced to the T10-11 vertebral level in urethane-anaesthetized rats. The effects of intrathecal (<em>i.t.</em>) injection of Tempol on mean arterial pressure (MAP), heart rate (HR), renal and splanchnic sympathetic nerve activity (rSNA and sSNA, respectively) were evaluated over 60 consecutive minutes. mRNA expression of enzymes involved in oxidative balance was analyzed in the spinal cord. In addition, spinal ROS abundance was quantified by the DHE fluorescence method. An increase in ROS production was observed in the thoracic region of 2K1C rats compared to the control group. <em>I.t.</em> administration of Tempol triggered a significant and preferential reduction in rSNA in the 2K1C but not in control rats. Thus, the data suggest that renal sympathoexcitation in 2K1C rats was associated with an increase in oxidative imbalance in the spinal cord, particularly in sympathetic preganglionic neurons that drive rSNA.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"868 ","pages":"Article 138408"},"PeriodicalIF":2.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233062","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

Combined chronic oral methylphenidate and fluoxetine treatment increases CB1 receptor density in the somatosensory forelimb region. 慢性口服哌甲酯和氟西汀联合治疗可增加躯体感觉前肢区域CB1受体密度。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-10-02 DOI: 10.1016/j.neulet.2025.138407

Abigail M Lantry, Huy Lu, Matt Marion, John Hamilton, Brittany Richardson, Teresa Quattrin, Lucy D Mastrandrea, Michael Hadjiargyrou, David Komatsu, Panayotis K Thanos

{"title":"Combined chronic oral methylphenidate and fluoxetine treatment increases CB1 receptor density in the somatosensory forelimb region.","authors":"Abigail M Lantry, Huy Lu, Matt Marion, John Hamilton, Brittany Richardson, Teresa Quattrin, Lucy D Mastrandrea, Michael Hadjiargyrou, David Komatsu, Panayotis K Thanos","doi":"10.1016/j.neulet.2025.138407","DOIUrl":"https://doi.org/10.1016/j.neulet.2025.138407","url":null,"abstract":"<p><p>Methylphenidate (MP) is a psychostimulant commonly prescribed for attention deficit hyperactivity disorder (ADHD), and Fluoxetine (FLX) is a Serotonin Selective Reuptake Inhibitor (SSRI) commonly prescribed to treat depression and anxiety disorders. Both are shown to impact neurochemistry and behavior, but little is known about their individual and combined impacts on the endocannabinoid system (ECS). We examined the effects of MP and FLX, both as separate treatments and in combination, on cannabinoid receptor type 1 (CB1) binding in several key brain regions of interest. Male rats were treated with either water, MP, FLX, or MP + FLX via a previously established drinking paradigm for three months. Brains were harvested, and [<sup>3</sup>H] SR141716A in vitro autoradiography was performed to quantify CB1 binding. The combined treatment of MP + FLX showed significantly higher [<sup>3</sup>H] SR141716A binding compared to the water, MP, and FLX groups in the somatosensory forelimb (S(FL)) region. This indicates an ability of the common co-usage of MP and FLX to increase CB1 levels in the somatosensory cortex: a region of the brain required for the processing of sensory information.</p>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":" ","pages":"138407"},"PeriodicalIF":2.0,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228286","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

Dexmedetomidine improves postoperative cognitive dysfunction via regulating Adrb2/Pkg: Dexmedetomidine against postoperative cognitive dysfunction. 右美托咪定通过调节Adrb2/Pkg改善术后认知功能障碍：右美托咪定抗术后认知功能障碍。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-10-01 DOI: 10.1016/j.neulet.2025.138406

Cuirong Chen, Hong Han, Hongzhe Li, Zitan Zhang, Yingbing Lv

{"title":"Dexmedetomidine improves postoperative cognitive dysfunction via regulating Adrb2/Pkg: Dexmedetomidine against postoperative cognitive dysfunction.","authors":"Cuirong Chen, Hong Han, Hongzhe Li, Zitan Zhang, Yingbing Lv","doi":"10.1016/j.neulet.2025.138406","DOIUrl":"10.1016/j.neulet.2025.138406","url":null,"abstract":"<p><strong>Background: </strong>Postoperative cognitive dysfunction (POCD) refers to postoperative neurological complications in patients, thus affecting patients' normal daily life.</p><p><strong>Purpose: </strong>Our study aimed to confirm whether Adrb2/Pkg are involved in the protective effect of Dexmedetomidine (Dex) against POCD in rats.</p><p><strong>Methods: </strong>The targets for Dex against POCD were screened by online databases. An POCD rat model was constructed, and the Morris water maze tests were conducted to evaluate the cognitive function of POCD rats. The inflammatory markers (IL-6, TNF-α, and IL-13) were recorded, and the levels of Adrb2 and Pkg in hippocampus tissue were detected using RT-qPCR. The key targets Adrb2/Pkg were verified through the LPS-induced inflammatory BV-2 cell model.</p><p><strong>Results: </strong>Network pharmacology analysis predicted that Adrb2 and Pkg were the key genes of Dex against POCD. Dex treatment improved learning and memory skills of POCD rats. In vitro and in vivo experiments showed that Dex treatment alleviated inflammation, and upregulated Adrb2 and Pkg mRNA levels of POCD rats and inflammatory BV-2 cell line. Silencing Adrb2/Pkg reversed the apoptosis suppression in LPS-induced inflammatory BV-2 cells caused by Dex.</p><p><strong>Conclusion: </strong>The Adrb2/Pkg could potentially be the mechanism by which Dex protects POCD rats from cognitive impairment.</p>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":" ","pages":"138406"},"PeriodicalIF":2.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225823","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

Hydrogen sulfide protects against hippocampal neuronal apoptosis in aged rats with postoperative cognitive dysfunction by promoting m6A methylation 硫化氢通过促进m6A甲基化对术后认知功能障碍老年大鼠海马神经元凋亡的保护作用。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-09-30 DOI: 10.1016/j.neulet.2025.138405

Bo Wang , YongPan Wen , Yonghong Tang , Min Li

{"title":"Hydrogen sulfide protects against hippocampal neuronal apoptosis in aged rats with postoperative cognitive dysfunction by promoting m6A methylation","authors":"Bo Wang , YongPan Wen , Yonghong Tang , Min Li","doi":"10.1016/j.neulet.2025.138405","DOIUrl":"10.1016/j.neulet.2025.138405","url":null,"abstract":"<div><h3>Purpose</h3><div>To explore the potential involvement of m6A methylation in the neuroprotective mechanism of H<sub>2</sub>S against hippocampus neuronal apoptosis in aged rats with POCD.</div></div><div><h3>Methods</h3><div>Sprague-Dawley rats (18–20 months) were subjected to anesthesia and laparotomy surgery to establish an animal model of POCD. The Open Field, Y-maze, and Novel Object Recognition tests assessed behavioral performance. Protein expression levels were analyzed using Western blot analysis, and neuronal apoptosis was analyzed using TUNEL staining.</div></div><div><h3>Results</h3><div>NaHS (100 μmol/kg) significantly increased the alternation ratio of the Y-maze test and the discrimination index of the NOR test, reduced hippocampal neuronal apoptosis, indicated by decreased TUNEL-positive neurons and modulated the expression of apoptosis-related protein markers (Bcl-2 was upregulated and Bax/Cleaved caspase-3 were downregulated). Furthermore, NaHS restored reduced m<sup>6</sup>A RNA methylation levels and corrected the disturbed expression of m<sup>6</sup>A-related enzymes (METTL3, METTL14, YTHDF1, YTHDF3, FTO, ALKBH5) in the hippocampus of aged rats with POCD.</div></div><div><h3>Conclusion</h3><div>H<sub>2</sub>S shows neuroprotective effects by mitigating hippocampal neuronal apoptosis and restoring m<sup>6</sup>A RNA methylation in the hippocampus of aged rats with POCD. These findings provide preclinical evidence that H<sub>2</sub>S may serve as a potential therapeutic agent for the prevention of POCD.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"868 ","pages":"Article 138405"},"PeriodicalIF":2.0,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213220","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

GABAergic disinhibition through the STING-dependent autophagic pathway in the dorsal horn underlies diabetic neuropathic pain pathogenesis 糖尿病神经性疼痛的发病机制是通过背角中sting依赖的自噬途径解除gaba能抑制。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-09-28 DOI: 10.1016/j.neulet.2025.138391

Ya-Jie Zhao , Hong-Zhen Bai , Yi-Na Wang , Yu-Kun Liu , Long-Biao Zhao , Zhao Li , Hui-Zhou Li , Xiu-Li Wang , Peng Liu

{"title":"GABAergic disinhibition through the STING-dependent autophagic pathway in the dorsal horn underlies diabetic neuropathic pain pathogenesis","authors":"Ya-Jie Zhao , Hong-Zhen Bai , Yi-Na Wang , Yu-Kun Liu , Long-Biao Zhao , Zhao Li , Hui-Zhou Li , Xiu-Li Wang , Peng Liu","doi":"10.1016/j.neulet.2025.138391","DOIUrl":"10.1016/j.neulet.2025.138391","url":null,"abstract":"<div><div>Our previous study demonstrated that STING/ATG5-mediated autophagy in the spinal dorsal horn contributes to diabetic neuropathic pain (DNP), although the underlying mechanisms remained unclear. In this study, we investigated how STING-driven autophagy leads to impaired spinal inhibition via lysosomal degradation of GABA receptors. In a rat model of DNP, spinal levels of STING and ATG5 were elevated, while P62, GABA<sub>A</sub> receptor, and GABA<sub>B</sub> receptor expression were reduced. Behavioral tests showed that intrathecal administration of a STING inhibitor increased mechanical pain thresholds and upregulated P62 and GABA receptors. Conversely, treatment with a STING agonist worsened hyperalgesia and further suppressed GABA receptor expression. Knockdown of ATG5 via siRNA similarly alleviated pain and restored GABA receptor levels. Interestingly, although the mTOR inhibitor rapamycin alleviated neuropathic pain, it unexpectedly increased spinal P62 expression compared to the DNP group. Administration of leupeptin, a lysosomal protease inhibitor, significantly increased paw withdrawal thresholds on days 1–3 and elevated GABA receptor expression, whereas the proteasomal inhibitor MG132 had no effect. These results demonstrate that STING/ATG5-mediated autophagy promotes DNP through autophagic-lysosomal degradation of GABA receptors, highlighting this pathway as a promising therapeutic target for treating diabetic neuropathic pain.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"868 ","pages":"Article 138391"},"PeriodicalIF":2.0,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200469","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

Cannabidiol engages the peripheral endogenous opioid system to produce analgesia in neuropathic mice 大麻二酚参与外周内源性阿片系统对神经病小鼠产生镇痛作用。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-09-27 DOI: 10.1016/j.neulet.2025.138393

Douglas Lamounier de Almeida , Walace Cássio Pinto Barra , Renata Cristina Mendes Ferreira , Flávia Cristina Fonseca , Daniel Portela Dias Machado , Danielle Diniz Aguiar , Francisco Silveira Guimaraes , Igor Dimitri Gama Duarte , Thiago Roberto Lima Romero

{"title":"Cannabidiol engages the peripheral endogenous opioid system to produce analgesia in neuropathic mice","authors":"Douglas Lamounier de Almeida , Walace Cássio Pinto Barra , Renata Cristina Mendes Ferreira , Flávia Cristina Fonseca , Daniel Portela Dias Machado , Danielle Diniz Aguiar , Francisco Silveira Guimaraes , Igor Dimitri Gama Duarte , Thiago Roberto Lima Romero","doi":"10.1016/j.neulet.2025.138393","DOIUrl":"10.1016/j.neulet.2025.138393","url":null,"abstract":"<div><div>Cannabidiol (CBD) has been getting attention from the scientific community regarding its potential for the treatment of different conditions, such as epilepsy, anxiety, and pain. This potential can be useful in clinical practice as an alternative or as an adjuvant alongside conventional therapeutic approaches; however, its mechanisms of action should be best described for its more effective application. Thus, our study aimed to evaluate whether the peripheral opioid system is involved in the analgesic mechanism of cannabidiol administered systemically for the treatment of neuropathic pain. Male <em>Swiss</em> mice were subjected to the sciatic constriction injury, and their nociceptive threshold was evaluated using the mechanical paw pressure test. Cannabidiol 20 mg/Kg produced an antinociceptive effect. Bestatin (400 µg/paw), a selective aminopeptidase-N inhibitor, potentiates the intermediate analgesic response of CBD at the dose of 2 mg/Kg. Naloxone (50 µg/paw), a non-selective opioid receptor antagonist, reversed the CBD-mediated analgesia. CTOP (5, 10, and 20 µg/paw) and naltrindole (30, 60, and 120 µg/paw), μ and Δ opioid receptor antagonists, but not norBNI (200 µg/paw), a κ opioid receptor antagonist, partially reversed the CBD analgesia. Thus, our study shows that cannabidiol may induce activation of opioid receptors in the periphery as a part of its analgesic mechanism in neuropathic pain.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"868 ","pages":"Article 138393"},"PeriodicalIF":2.0,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192180","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

Relationship between prefrontal oxygenation during task-set period and executive function in healthy older people: A near-infrared spectroscopy study 健康老年人任务设定期前额叶氧合与执行功能的关系：近红外光谱研究

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-09-27 DOI: 10.1016/j.neulet.2025.138395

Yumi Oboshi , Mitsuru Kikuchi , Yasuomi Ouchi

{"title":"Relationship between prefrontal oxygenation during task-set period and executive function in healthy older people: A near-infrared spectroscopy study","authors":"Yumi Oboshi , Mitsuru Kikuchi , Yasuomi Ouchi","doi":"10.1016/j.neulet.2025.138395","DOIUrl":"10.1016/j.neulet.2025.138395","url":null,"abstract":"<div><h3>Introduction</h3><div>In past research, we have examined the characteristics of brain activity caused by prefrontal task completion in healthy older adults in a simplified manner using a near-infrared spectroscopy device, with the aim of identifying methods of early intervention to prevent their cognitive decline. Previously, we reported that prefrontal oxygenation during pre-task preparation was greater in young adults than older adults, and that this greater activation was associated with better task performances in both groups. To extend this research, in the present study, we examined previous findings with task repetitions, as older adults take more time to become familiar new tasks.</div></div><div><h3>Methods</h3><div>We modified the working memory task with a clear task-set instruction and examined the change in the task-set and task-induced activation in 63 cognitively healthy older adults.</div></div><div><h3>Results</h3><div>Task-set activation did not increase even after three repetitions, and the task-induced activation was greater than task-set activation in most channels. The difference in degree between task-induced activation and task-set activation showed a reduction with task repetitions. Significant inverse correlations were observed between the prefrontal activation due to the task itself in the third session, i.e., after task repetitions and the reaction time of the Trail Making Test, which represents attentional function.</div></div><div><h3>Discussion</h3><div>These results indicate that continued activation by the task itself, which persists even after older adults become familiar with the task, may be associated with executive function decline.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"868 ","pages":"Article 138395"},"PeriodicalIF":2.0,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192258","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

Nicotine exacerbates fear and depression-like behaviors by promoting microglial phagocytosis of synaptic protein in a mouse model of foot shock 在足震小鼠模型中，尼古丁通过促进突触蛋白的小胶质吞噬而加剧恐惧和抑郁样行为。

IF 2 4区医学

Neuroscience Letters Pub Date : 2025-09-25 DOI: 10.1016/j.neulet.2025.138394

Jiaquan Wang , Xiao-kang Gong , Jing Yu , Liangwei Wu , Yuheng Zhang , Pan Li , Min Qin , Xiao-chuan Wang , Xi-ji Shu , Jian Bao

{"title":"Nicotine exacerbates fear and depression-like behaviors by promoting microglial phagocytosis of synaptic protein in a mouse model of foot shock","authors":"Jiaquan Wang , Xiao-kang Gong , Jing Yu , Liangwei Wu , Yuheng Zhang , Pan Li , Min Qin , Xiao-chuan Wang , Xi-ji Shu , Jian Bao","doi":"10.1016/j.neulet.2025.138394","DOIUrl":"10.1016/j.neulet.2025.138394","url":null,"abstract":"<div><div>Post-traumatic stress disorder (PTSD) is a severe psychiatric disorder characterized by a complex interplay of genetic and environmental influences. Substantial evidence has demonstrated an intricate nexus between nicotine, the principal psychoactive constituent of cigarette smoke, and PTSD neuropathology. Nevertheless, the intricate mechanism underlying the relationship between nicotine consumption and PTSD has not yet been fully understood. Following two weeks of intraperitoneal nicotine administration at two doses (5 mg/kg and 1 mg/kg), we initiated behavioral testing. Our findings reveal that nicotine supplementation exacerbates fear and depression-like behaviors while promoting microglial phagocytosis of synaptic proteins. Moreover, we observed synaptic protein loss and microglial activation in both the hippocampus and cortex in the 5 mg/kg group. CX3CR1-Cre driven Cre recombinase (Cre) is a widely used genetic tool for enabling gene manipulation in microglia. Here, we investigated a genetic ablation method of the CX3CR1 using a Cre-responsive adeno-associated virus (AAV) vector expressing diphtheria toxin subunit-A (DTA). Conversely, microglial ablation via rAAV-EF1a-DIO-DTA-WPRE hGH pA injection in the ventral hippocampus CA1 region of CX3CR1-Cre mice appears to mitigate the pathologies and behavioral abnormalities induced by nicotine. Our results underscore the role of nicotine in the progression of PTSD and demonstrate that microglial depletion mitigates nicotine-induced pathologies and behavioral disturbances. Consequently, our findings suggest that nicotine enhances microglial phagocytosis of synaptic proteins in PTSD, thereby exacerbating fear and depressive symptoms.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"867 ","pages":"Article 138394"},"PeriodicalIF":2.0,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182020","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