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Fluorescent Sensor for the Visualization of Amino Acid Neurotransmitters in Neurons Based on an SNAr Reaction
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-11 DOI: 10.1021/acschemneuro.5c0010710.1021/acschemneuro.5c00107
Ming Xu, Peeyush Yadav, Xin Liu, Kevin D. Gillis* and Timothy E. Glass*, 
{"title":"Fluorescent Sensor for the Visualization of Amino Acid Neurotransmitters in Neurons Based on an SNAr Reaction","authors":"Ming Xu,&nbsp;Peeyush Yadav,&nbsp;Xin Liu,&nbsp;Kevin D. Gillis* and Timothy E. Glass*,&nbsp;","doi":"10.1021/acschemneuro.5c0010710.1021/acschemneuro.5c00107","DOIUrl":"https://doi.org/10.1021/acschemneuro.5c00107https://doi.org/10.1021/acschemneuro.5c00107","url":null,"abstract":"<p >Glutamate is an important excitatory neurotransmitter, while GABA is an inhibitory neurotransmitter. However, direct and accurate visualization of these important signaling agents by a chemical sensor is still very challenging. Here, a novel coumarin-based fluorescent sensor for the selective labeling and imaging of amino acids in neurons has been developed. This sensor system provides two binding sites for amino acids: an aldehyde group for the amine binding and a modified fluorobenzene for an unusual nucleophilic aromatic substitution (S<sub>N</sub>Ar) reaction of a carboxyl group. Spectroscopic studies reveal a large fluorescence enhancement upon reaction with glutamate. Compounds lacking both groups did not activate the sensor. A clear and efficient visualization of neurotransmitters in cultured hippocampus neurons was obtained by imaging studies.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"16 6","pages":"1238–1242 1238–1242"},"PeriodicalIF":4.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143641567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Neurochemical Assessment of Tissue Levels of Neurotransmitters for Approximating Neurotransmitter System Connectivity.
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-11 DOI: 10.1021/acschemneuro.5c00060
Jasmine Jade Butler, Chloé Aman, Marion Rivalan, Aurélie Fitoussi, Sandrine Parrot, Françoise Dellu-Hagedorn, Philippe De Deurwaerdère
{"title":"Neurochemical Assessment of Tissue Levels of Neurotransmitters for Approximating Neurotransmitter System Connectivity.","authors":"Jasmine Jade Butler, Chloé Aman, Marion Rivalan, Aurélie Fitoussi, Sandrine Parrot, Françoise Dellu-Hagedorn, Philippe De Deurwaerdère","doi":"10.1021/acschemneuro.5c00060","DOIUrl":"https://doi.org/10.1021/acschemneuro.5c00060","url":null,"abstract":"<p><p>The post-mortem measurement of tissue neurotransmitters is an interesting technique to address the gross biochemical activity. Its primary limitation is a lack of temporal resolution, although this is mitigated by enhanced spatial resolution, compared to <i>in vivo</i> methods. This neurochemical data is quantitative and requires no complex transformation, making it ideal to analyze neurochemical connectivity via the correlation of the biochemical signals between brain regions. These correlative approaches to quantitative measurements are fundamentally based on the variability of the data, an underdeveloped area of analysis in neurochemistry. One of the main reasons, as discussed in this Viewpoint, is that neurochemists recognize that variability in quantitative data stems not only from the biological variability, such as interindividual differences, but also from factors such as analytical devices. There are several ways to reduce variability caused by analytical and experimental biases through well-designed, precise protocols, allowing for the study of meaningful biological variability, such as interindividual differences between subjects.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143602960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Radiosynthesis, In Vitro Characterization, and In Vivo PET Neuroimaging of [18F]F-4 for Tau Protein: A First-in-Human PET Study
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-10 DOI: 10.1021/acschemneuro.4c0086610.1021/acschemneuro.4c00866
Anton Lindberg, Junchao Tong, Chao Zheng, Andre Mueller, Heiko Kroth, Andrew Stephens, Chester A. Mathis and Neil Vasdev*, 
{"title":"Radiosynthesis, In Vitro Characterization, and In Vivo PET Neuroimaging of [18F]F-4 for Tau Protein: A First-in-Human PET Study","authors":"Anton Lindberg,&nbsp;Junchao Tong,&nbsp;Chao Zheng,&nbsp;Andre Mueller,&nbsp;Heiko Kroth,&nbsp;Andrew Stephens,&nbsp;Chester A. Mathis and Neil Vasdev*,&nbsp;","doi":"10.1021/acschemneuro.4c0086610.1021/acschemneuro.4c00866","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00866https://doi.org/10.1021/acschemneuro.4c00866","url":null,"abstract":"<p >[<sup>18</sup>F]PI-2620 is a promising radiopharmaceutical for positron emission tomography (PET) imaging of both Alzheimer’s disease (AD) and non-Alzheimer’s disease (non-AD) tauopathies in humans. An array of fluorinated derivatives of the carbazole scaffold of PI-2620 were synthesized and evaluated. <i>In vitro</i> binding assays with [<sup>3</sup>H]PI-2620 in human tissues with AD, progressive supranuclear palsy, and corticobasal degeneration, combined with <i>in silico</i> predictions of blood–brain barrier permeability, led to the selection and radiosynthesis of [<sup>18</sup>F]F-4 as a promising radiotracer. <i>In vivo</i> PET imaging with [<sup>18</sup>F]F-4 in healthy rats showed brain uptake and kinetics suitable for neuroimaging, similar to those of [<sup>18</sup>F]PI-2620. A first-in-human PET imaging study in a healthy subject as well as a patient with AD, in comparison with [<sup>18</sup>F]PI-2620 in the same AD subject, confirmed that [<sup>18</sup>F]F-4 is an alternative radiopharmaceutical for imaging tau protein.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"16 6","pages":"1182–1189 1182–1189"},"PeriodicalIF":4.1,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acschemneuro.4c00866","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143641550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 Use of Natural Volatile Compounds on the Fibrillation Domain of Amyloid Beta (GSNKGAIIGLM)─Towards Promising Agents to Combat Alzheimer’s Disease
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-09 DOI: 10.1021/acschemneuro.4c0076810.1021/acschemneuro.4c00768
Zahra Dindar, Afrooz Anbaraki, Seyyed Sina Hosseini, Zohreh Harati, Aida Bahrami, Saeed Balalaie, Maryam Ghobeh, Majid Mahdavi and Arefeh Seyedarabi*, 
{"title":"The Use of Natural Volatile Compounds on the Fibrillation Domain of Amyloid Beta (GSNKGAIIGLM)─Towards Promising Agents to Combat Alzheimer’s Disease","authors":"Zahra Dindar,&nbsp;Afrooz Anbaraki,&nbsp;Seyyed Sina Hosseini,&nbsp;Zohreh Harati,&nbsp;Aida Bahrami,&nbsp;Saeed Balalaie,&nbsp;Maryam Ghobeh,&nbsp;Majid Mahdavi and Arefeh Seyedarabi*,&nbsp;","doi":"10.1021/acschemneuro.4c0076810.1021/acschemneuro.4c00768","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00768https://doi.org/10.1021/acschemneuro.4c00768","url":null,"abstract":"<p >Alzheimer’s disease (AD), which is caused by the accumulation of amyloid-beta, is a major medical concern today. Controlling these aggregates is critical to drug development, but delivering them effectively into the bloodstream poses significant challenges. In this context, aromatherapy has been proposed as an innovative and promising approach for AD disease. The volatile compounds cinnamaldehyde, phenylethyl alcohol, α-asarone, and β-caryophyllene have neuroprotective effects that can be effective in the treatment of neurodegenerative diseases like AD. The amyloid-beta (Aβ) fragment (25–35), which retains the properties of the full-length Aβ is used as a suitable model to evaluate the potential toxicity associated with AD. This study investigated the effects of the four mentioned volatile compounds at four different concentrations on the fibrillation process of the Aβ (25–35) peptide. Structural changes in the peptide have been analyzed using various techniques such as fluorescence probing, far-UV circular dichroism spectroscopy (CD), and atomic force microscopy (AFM). Fluorescence probing results showed that these compounds can effectively prevent the formation of amyloid fibrils by forming chemical bonds with the intermediate species. CD spectroscopy results indicated a decrease in β-sheet content of fibrils and confirmed the effect of pH on structural changes. AFM analysis revealed that volatile compounds effectively prevented the formation of amyloid fibrils at different concentrations and changed the average size of intermediates and oligomeric species. These findings show a promising future for AD patients and emphasize the importance of natural compounds in the treatment and prevention of neurodegenerative diseases.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"16 6","pages":"1086–1102 1086–1102"},"PeriodicalIF":4.1,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143641689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Cytotoxicity of Amyloid β1–42 Fibrils to Brain Immune Cells
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-08 DOI: 10.1021/acschemneuro.4c0083510.1021/acschemneuro.4c00835
Mikhail Matveyenka, Mikhail Sholukh and Dmitry Kurouski*, 
{"title":"Cytotoxicity of Amyloid β1–42 Fibrils to Brain Immune Cells","authors":"Mikhail Matveyenka,&nbsp;Mikhail Sholukh and Dmitry Kurouski*,&nbsp;","doi":"10.1021/acschemneuro.4c0083510.1021/acschemneuro.4c00835","DOIUrl":"https://doi.org/10.1021/acschemneuro.4c00835https://doi.org/10.1021/acschemneuro.4c00835","url":null,"abstract":"<p >Alzheimer’s disease (AD) is a progressive pathology that is linked to abrupt aggregation of amyloid β<sub>1–42</sub> (Aβ<sub>1–42</sub>) peptide in the central nervous system. Aβ<sub>1–42</sub> aggregation yields amyloid oligomers and fibrils, toxic protein aggregates that cause progressive neuronal degeneration in the frontal lobe of the brain. Although neurons remain the focus of AD for decades, a growing body of evidence suggests that the degeneration of immune cells in the brain can be the major cause of AD. However, the extent to which Aβ<sub>1–42</sub> aggregates are toxic to the major classes of immune cells in the brain remains unclear. In the current study, we examine the cytotoxic effects of Aβ<sub>1–42</sub> fibrils on macrophages, dendritic cells, and microglia. These cells play vitally important roles in development and homeostasis of the central nervous system. We found that Aβ<sub>1–42</sub> fibrils caused calcium release and enhanced levels of reactive oxygen species in macrophages, dendritic cells, and microglia as well as neurons. We also investigated the extent to which the lysozymes of these immune cells could alter the aggregation properties of Aβ<sub>1–42</sub>. Our results showed that lysosomes extracted from macrophages, dendritic cells, and microglia drastically accelerated Aβ<sub>1–42</sub> aggregation as well as altered cytotoxicity of these protein aggregates. These results indicate that impairment of immune cells in the brain can be a critically important aspect of neurodegenerative processes that are taking place upon the onset of AD.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"16 6","pages":"1144–1149 1144–1149"},"PeriodicalIF":4.1,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acschemneuro.4c00835","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143641613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Corilagin Attenuates Neuronal Apoptosis and Ferroptosis of Parkinson's Disease through Regulating the TLR4/Src/NOX2 Signaling Pathway. 柯里拉京通过调节TLR4/Src/NOX2信号通路减轻帕金森病的神经元凋亡和铁凋亡
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-05 Epub Date: 2025-02-14 DOI: 10.1021/acschemneuro.5c00035
Yu Lei, Jiabin Zhou, Dongyuan Xu, Songshan Chai, Nanxiang Xiong
{"title":"Corilagin Attenuates Neuronal Apoptosis and Ferroptosis of Parkinson's Disease through Regulating the TLR4/Src/NOX2 Signaling Pathway.","authors":"Yu Lei, Jiabin Zhou, Dongyuan Xu, Songshan Chai, Nanxiang Xiong","doi":"10.1021/acschemneuro.5c00035","DOIUrl":"10.1021/acschemneuro.5c00035","url":null,"abstract":"<p><p>Corilagin has shown neuroprotective potential in various neurological disorders, but its effects in Parkinson's disease (PD) have not been fully explored. In this study, we investigated the therapeutic impact and underlying mechanism of corilagin on PD using MPTP-induced mice and MPP<sup>+</sup>-treated N2a cells. Behavioral tests and immunohistochemical analysis demonstrated that corilagin significantly reduced MPTP-induced loss of TH-positive neurons in the substantia nigra. In vitro, corilagin improved cell viability, decreased MPP<sup>+</sup>-induced apoptosis, and mitigated the associated oxidative stress by lowering intracellular ROS levels and preserving mitochondrial membrane potential. Moreover, corilagin reversed MPP<sup>+</sup>-induced iron accumulation and lipid peroxidation in N2a cells. Mechanistically, Western blotting revealed that the protective effects of corilagin are linked to the TLR4/Src/NOX2 signaling pathway. The TLR4 agonist RS 09 impaired the neuroprotective effects of corilagin, further supporting its role in modulating ferroptosis via this pathway. These findings suggest that corilagin could be a promising therapeutic agent for PD by targeting the TLR4/Src/NOX2 signaling axis to inhibit ferroptosis.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":" ","pages":"968-980"},"PeriodicalIF":4.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Enhanced Cognitive and Memory Functions via Gold Nanoparticle-Mediated Delivery of Afzelin through Synaptic Modulation Pathways in Alzheimer's Disease Mouse Models.
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-05 Epub Date: 2025-02-20 DOI: 10.1021/acschemneuro.4c00766
Ju Hee Mun, Min Jun Jang, Won Seok Kim, Seong-Seop Kim, Bonggi Lee, HyunSeon Moon, Soo-Jin Oh, Cheol-Hui Ryu, Kyung Su Park, Ik-Hyun Cho, Gyu-Sang Hong, Chun Whan Choi, Changhyuk Lee, Min Soo Kim
{"title":"Enhanced Cognitive and Memory Functions via Gold Nanoparticle-Mediated Delivery of Afzelin through Synaptic Modulation Pathways in Alzheimer's Disease Mouse Models.","authors":"Ju Hee Mun, Min Jun Jang, Won Seok Kim, Seong-Seop Kim, Bonggi Lee, HyunSeon Moon, Soo-Jin Oh, Cheol-Hui Ryu, Kyung Su Park, Ik-Hyun Cho, Gyu-Sang Hong, Chun Whan Choi, Changhyuk Lee, Min Soo Kim","doi":"10.1021/acschemneuro.4c00766","DOIUrl":"10.1021/acschemneuro.4c00766","url":null,"abstract":"<p><p>Gold nanoparticles (AuNPs) are valuable tools in pharmacological and biological research, offering unique properties for drug delivery in the treatment of neurodegenerative diseases. This study investigates the potential of gold nanoparticles loaded with afzelin, a natural chemical extracted from <i>Ribes fasciculatum</i>, to enhance its therapeutic effects and overcome the limitations of using natural compounds regarding low productivity. We hypothesized that the combined treatment of AuNPs with afzelin (AuNP-afzelin) would remarkably enforce neuroprotective effects compared with the single treatment of afzelin. Central administration of AuNP-afzelin (10 ng of afzelin) indicated improvements in cognition and memory-involved assessments of behavioral tests, comparing single treatments of afzelin (10 or 100 ng of afzelin) in scopolamine-induced AD mice. AuNP-afzelin also performed superior neuroprotective effects of rescuing mature neuronal cells and recovered cholinergic dysfunction compared to afzelin alone, according to further investigations of BDNF-pCREB-pAkt signaling, long-term potentiation, and doublecortin (DCX) expression in the hippocampus. This study highlights the potential of afzelin with gold nanoparticles as a promising therapeutic approach for mitigating cognitive impairments associated with neurodegenerative diseases and offers a new avenue for future research and drug development.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":" ","pages":"826-843"},"PeriodicalIF":4.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
M4 Positive Allosteric Modulator VU0467154 Impacts Amphetamine Sensitization and Spontaneous Locomotion in Male Mice.
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-05 Epub Date: 2025-02-21 DOI: 10.1021/acschemneuro.4c00795
Anna Berezovskaia, Craig Lindsley, Anders Fink-Jensen, Gitta Wörtwein
{"title":"M<sub>4</sub> Positive Allosteric Modulator VU0467154 Impacts Amphetamine Sensitization and Spontaneous Locomotion in Male Mice.","authors":"Anna Berezovskaia, Craig Lindsley, Anders Fink-Jensen, Gitta Wörtwein","doi":"10.1021/acschemneuro.4c00795","DOIUrl":"10.1021/acschemneuro.4c00795","url":null,"abstract":"<p><p>This study investigates the effects of the muscarinic acetylcholine receptor subtype 4 (M<sub>4</sub>) positive allosteric modulator (PAM) VU0467154 on the development, incubation, and expression of amphetamine sensitization in mice, the expression of immediate early genes in the medial prefrontal cortex after induction and expression of sensitization, as well as on spontaneous locomotion and several aspects of sensorimotor function. Mice were pretreated with VU0467154 during the induction phase, before the challenge test, or both. A separate cohort was treated during the incubation period. Tests of spontaneous locomotion and sensorimotor function were conducted after VU0467154 administration to evaluate potential side effects. Treatment with VU0467154 inhibited the development and expression of amphetamine sensitization. This was paralleled by effects on immediate early gene expression in the medial prefrontal cortex. Additionally, previous pretreatment with VU0467154 during the induction phase attenuated the expression of sensitization after a two-week incubation period. However, treatment with VU0467154 during the incubation period did not affect the expression of a sensitized response. VU0467154 significantly reduced spontaneous locomotion without impairing other aspects of sensorimotor function, as assessed by the mesh, adhesive removal, horizontal bar, and negative geotaxis tests. Global M<sub>4</sub> knockout mice confirmed that the inhibitory effect on spontaneous locomotion was specific to M<sub>4</sub> receptors. Our findings provide new insights into the therapeutic potential of M<sub>4</sub> PAMs in modulating the neuroadaptations associated with psychostimulant abuse. Collectively, these results suggest that activation of M<sub>4</sub> receptors could be a promising strategy for modulating dopaminergic signaling and reducing some behaviors associated with substance use disorder.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":" ","pages":"868-879"},"PeriodicalIF":4.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Anterior Cingulate Cortex-Anterior Insular Cortex Circuit Mediates Hyperalgesia in Adolescent Mice Experiencing Early Life Stress.
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-05 Epub Date: 2025-02-17 DOI: 10.1021/acschemneuro.4c00884
Meng Li, Kefang Liu, Mingyu Xu, Zhaoyi Chen, Lu Yu, Jingquan Zhang, Chunyan Wang, Cheng Long, Jinxiang Jiang
{"title":"Anterior Cingulate Cortex-Anterior Insular Cortex Circuit Mediates Hyperalgesia in Adolescent Mice Experiencing Early Life Stress.","authors":"Meng Li, Kefang Liu, Mingyu Xu, Zhaoyi Chen, Lu Yu, Jingquan Zhang, Chunyan Wang, Cheng Long, Jinxiang Jiang","doi":"10.1021/acschemneuro.4c00884","DOIUrl":"10.1021/acschemneuro.4c00884","url":null,"abstract":"<p><p>Understanding neurobiological mechanisms underlying changes in behavior and neural activity caused by early life stress (ELS) is essential for improving these adverse outcomes in individuals. ELS incited by exposure to maternal separation (MS) can be defined as a form of social pain, but little is known about the neural mechanism in adolescents with ELS-induced pain sensitization. Employing an MS-induced ELS paradigm in mice, we reported here that both male and female MS mice aged 1-2 months exhibited mechanical and thermal hyperalgesia using paw-withdrawal and hot/cold plate tests. The increased high gamma (γ<sub>high</sub>) oscillations accompanied by the activation of parvalbumin-positive interneurons (PVINs) in the anterior insular cortex (AIC), but not the anterior cingulate cortex (ACC), were shown in MS mice. Moreover, ACC-driven AIC connectivity was enhanced in MS mice, characterized by amplified phase coherence in the delta (δ) and theta (θ) bands and an escalation in the coupling of the ACC θ phase and AIC γ amplitude. Chemogenetic inactivation of AIC PVINs relieved hyperalgesia and altered the ACC-AIC connectivity in MS mice. The observed increase in δ-θ synchronization and PVIN activation in the ACC-AIC circuit indicates this pathway is a therapeutic target for ELS-induced hyperalgesia.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":" ","pages":"920-931"},"PeriodicalIF":4.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143431902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Correction to "Remote Ischemic Postconditioning-Mediated Neuroprotection against Stroke by Promoting Ketone Body-Induced Ferroptosis Inhibition".
IF 4.1 3区 医学
ACS Chemical Neuroscience Pub Date : 2025-03-05 Epub Date: 2025-02-12 DOI: 10.1021/acschemneuro.5c00051
Lin-Yan Huang, Yi-de Zhang, Yi-Ning Liu, Zhi-Yan Liang, Jie Chen, Bin Wang, Qi-Long Yin, Pei-Pei Wang, Wan Wang, Su-Hua Qi
{"title":"Correction to \"Remote Ischemic Postconditioning-Mediated Neuroprotection against Stroke by Promoting Ketone Body-Induced Ferroptosis Inhibition\".","authors":"Lin-Yan Huang, Yi-de Zhang, Yi-Ning Liu, Zhi-Yan Liang, Jie Chen, Bin Wang, Qi-Long Yin, Pei-Pei Wang, Wan Wang, Su-Hua Qi","doi":"10.1021/acschemneuro.5c00051","DOIUrl":"10.1021/acschemneuro.5c00051","url":null,"abstract":"","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":" ","pages":"981"},"PeriodicalIF":4.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
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