ACS Chemical Neuroscience最新文献

{"title":"Flexible Multimodal Neural Probe with Integrated Three-Electrode Aptameric Sensing for In Vivo Monitoring of Dopamine Dynamics and Neural Activity","authors":"Szu-Ying Li,&nbsp;Yun-Ting Kuo,&nbsp;Sheng-Huang Lin,&nbsp;Shun-An Kan,&nbsp;Bo-Wei Chen,&nbsp;Ssu-Ju Li,&nbsp;Ching-Wen Chang,&nbsp;Han-Lin Wang,&nbsp;Yu-Chun Lo,&nbsp;You-Yin Chen","doi":"10.1021/acschemneuro.6c00550","DOIUrl":"https://doi.org/10.1021/acschemneuro.6c00550","url":null,"abstract":"<p>Neural function emerges from the interplay between electricalactivityand neurochemical signaling, yet most implantable neural interfacesprimarily record electrophysiological signals and lack molecular specificityfor neurotransmitter monitoring. Here, we developed a flexible multimodalneural probe integrating an on-chip three-electrode electrochemicalaptamer sensor with electrophysiological recording sites for combinedmonitoring of extracellular dopamine (DA) dynamics and neuronal activity.Fabrication of the electrochemical interface was systematically optimizedby controlling gold nanostructure (AuNS) electrodeposition from 0.50to 0.70 V. Electrodeposition at 0.65 V provided the best balance betweenincreased electrochemically active surface area (ECSA), surface morphology,fabrication reproducibility, and electrical isolation, yielding anapproximately 4.7-fold ECSA enhancement with a probe-to-probe coefficientof variation (CV%) of 2.02%. A methylene blue-labeled DA aptamer wasassembled onto the AuNS working electrodes for sequence-specific molecularrecognition, while integrated Ag/AgCl reference and nanostructuredplatinum counter electrodes completed the on-chip sensing system.Electrochemical impedance analysis further demonstrated reproducibleinterfacial characteristics following stepwise functionalization.The electrophysiological electrodes exhibited a mean impedance of366.02 ± 18.63 kΩ at 1 kHz with an interprobe CV% of 5.09%.Square-wave voltammetry frequency was experimentally optimized from10 to 200 Hz, with 100 Hz providing the best balance between analyticalresponse, background current, and reproducibility. Under optimizedconditions, the sensor demonstrated sequence-specific DA recognition,selectivity against electroactive interferents, and an experimentallydetermined detection limit of 10 fM. Two absolute linear responseregions were identified at 0.5–10 pM (<em>R</em>² = 0.9945) and 0.5–10 nM (<em>R</em>² = 0.9949), while the broader detectable concentration range extendedfrom 10 fM to 1 μM. Flow-injection and brain-phantom experimentsdemonstrated reversible DA sensing. In acute rat caudate-putamen experiments,intravenous nomifensine induced DA-associated electrochemical responsesaccompanied by increased neuronal firing and γ/high-γlocal field potential activity, supporting this platform for acutemultimodal neurochemical and electrophysiological interrogation <em>in vivo</em>.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 16","pages":"3122–3149"},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148769642","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}

{"title":"Engineering ApoE3-Targeted NIR-Responsive Liposomes for Multimodal Inhibition of Amyloid-β Aggregation and Acetylcholinesterase Activity","authors":"Shubham Kumar Singh,&nbsp;Harsh Dinodiya,&nbsp;Shivay Parihar,&nbsp;Chiranjeevi Korupalli,&nbsp;Raviraj Vankayala","doi":"10.1021/acschemneuro.6c00315","DOIUrl":"https://doi.org/10.1021/acschemneuro.6c00315","url":null,"abstract":"<p>Alzheimer’s disease (AD) is characterized by progressiveneurodegeneration and cognitive decline, largely driven by amyloid-β(Aβ) aggregation and dysregulated acetylcholinesterase (AChE)activity. While current pharmacological interventions utilize AChEinhibitors and Aβ antagonists, their efficacy is frequentlyhampered by monotherapeutic limitations, poor blood–brain barrier(BBB) permeability, and a lack of controlled release mechanisms. Herein,we report the engineering of the liposomal formulation coloaded withDonepezil (DNP) and the photothermal agent indocyanine green (ICG),followed by conjugation of ApoE3 protein (LIDA) designed for multimodalAD therapy. Surface-conjugated ApoE3 serves a bifunctional role byfacilitating BBB penetration and actively inhibiting Aβ oligomerization.Upon 808 nm laser irradiation, ICG-mediated photothermal inductiontriggers the spatiotemporal release of DNP, significantly enhancingAChE inhibition. Furthermore, LIDA treatment effectively mitigatesAβ-induced cytotoxicity and mitochondrial dysfunction in SH-SY5Ycells. By integrating targeted delivery with NIR responsiveness, thisstudy presents a novel, multivalent strategy to combat the complexpathological landscape of AD.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 16","pages":"3094–3108"},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148769599","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}

{"title":"Serotonin Deficits Modulate Hippocampal Plasticity","authors":"Rocío B. Foltran,&nbsp;Mariano Soiza-Reilly","doi":"10.1021/acschemneuro.6c00120","DOIUrl":"10.1021/acschemneuro.6c00120","url":null,"abstract":"<p>Serotonin (5-HT) modulates a wide variety of functionsacross thecentral nervous systems. It is a key regulator of neuroplasticity,particularly in the hippocampus, where increased serotonergic signalinggenerally enhances the plasticity processes. However, the consequencesof 5-HT deficiency on brain plasticity remain poorly understood, whichis essential for clarifying the role of 5-HT in the etiology and treatmentof psychiatric disorders. Here, we survey findings from pharmacologicaland genetic models of 5-HT depletion, focusing on molecular, cellular,and neural circuit changes in the hippocampus, alongside related phenotypes.Evidence indicates that lowering 5-HT levels differentially impactsthe distinct forms of plasticity. While chronic depletion frequentlyincreases molecular plasticity markers, dendritic spines, and neurogenesis,it simultaneously impairs neural circuit plasticity and hippocampus-dependentmemory. In contrast, both acute and developmental 5-HT depletion consistentlyreduce both the structural and functional neuronal plasticity of thehippocampus. These findings highlight that the effects of 5-HT deficiencyare highly dependent on the timing, duration, and developmental stagesof the manipulation. Deconstructing this complexity is critical tointerpreting how reduced 5-HT levels alter hippocampal plasticityand contribute to psychiatric pathophysiology.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 16","pages":"3035–3047"},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148409686","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}

{"title":"Phage Display-Derived Cyclic Peptides Target TREM2 and Modulate Microglial Responses Under Amyloid Stress","authors":"Natalie Fuchs,&nbsp;Shaoren Yuan,&nbsp;Katarzyna Kuncewicz,&nbsp;Mohamed Atta Elhamouly,&nbsp;Farida El Gaamouch,&nbsp;Moustafa T. Gabr","doi":"10.1021/acschemneuro.6c00304","DOIUrl":"https://doi.org/10.1021/acschemneuro.6c00304","url":null,"abstract":"<p>Triggering receptor expressed on myeloid cells 2 (TREM2)is a keyregulator of microglial function and a promising therapeutic targetin Alzheimer’s disease. While current strategies have largelyfocused on antibody-based agonists, alternative modalities capableof modulating TREM2 signaling remain underexplored. Here, we reportthe discovery of TREM2-binding cyclic peptides using a disulfide-constrainedphage display library. Screening and biophysical validation identifiedmultiple binders, with <strong>TREM2–6</strong> and <strong>TREM2–12</strong> exhibiting micromolar affinity. Both peptides modulated microglialresponses in human iPSC-derived model of amyloid stress and in neuron-microgliacocultures. Molecular dynamics simulations supported stable peptide-TREM2interactions, with <strong>TREM2–12</strong> displaying a moreconstrained binding mode. In vitro pharmacokinetic profiling revealedfavorable plasma and intestinal stability but limited permeability,consistent with cyclic peptide scaffolds. Together, these findingsestablish cyclic peptides as a viable modality for targeting TREM2and provide a foundation for the development of tunable neuroimmunetherapeutics.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 16","pages":"3082–3093"},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148769854","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}

{"title":"The Role of PolyQ in Global Conformational Dynamics and Stability of Huntingtin","authors":"Girish Parmar,&nbsp;Kharerin Hungyo","doi":"10.1021/acschemneuro.6c00010","DOIUrl":"https://doi.org/10.1021/acschemneuro.6c00010","url":null,"abstract":"<p>Huntington’s disease (HD) is known for its abnormalpolyQstretch in the first exon of the HTT gene. HD is listed among thefatal autosomal dominant neurodegenerative disorders targeting thecentral nervous system and interfering with motor, cognitive, andpsychiatric functions. The HTT gene codes for Huntingtin (Htt), alarge three-domain protein with a polyQ stretch present in the N-terminaldomain. In diseased cells, inclusion bodies are enriched in Htt fragmentscontaining an extended polyQ region. The expansion of the polyQ correlateswith aggregate size and onset of HD. However, the exact role of thefull-length Htt in aggregate formation has not been fully known. Usingcoarse-grained molecular dynamics simulations at the near-atom level,our study indicates that the conformational dynamics of Htt─twistingand open-close motions of the domains─are dependent on thelength of polyQ. In the presence of HAP40, the global conformationallandscape is restricted, and the degree of dependence on polyQ lengthis low. The intra- and intercontact analyses suggest that the polyQregion can loop like a hairpin with a higher probability for a largerpolyQ length. However, the looping probability is reduced in the presenceof HAP40 due to increased contacts between polyQ and other regionsof Htt. Thus, our findings indicate that polyQ has a significant rolein the disease’s pathogenesis, which includes altered functionalactivity and structural modifications leading to inclusion body formation.These effects can be controlled with the help of HAP40.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 16","pages":"3058–3069"},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148769520","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}

{"title":"Structure–Property Relationship Analysis of α-Keto Ester Prodrugs of Monomethyl Fumarate as NRF2 Activators","authors":"Damian L. Stachura,&nbsp;Fátima Rivera-Escalera,&nbsp;Dion J. L. Turner,&nbsp;Mohd S.U. Rasheed,&nbsp;David M. Ruiz,&nbsp;Thomas D. Avery,&nbsp;Anibal R. Davalos,&nbsp;R. Jason Herr,&nbsp;Peter M. Grace,&nbsp;Andrew D. Abell","doi":"10.1021/acschemneuro.6c00139","DOIUrl":"10.1021/acschemneuro.6c00139","url":null,"abstract":"<p>The transcription factor nuclear factor erythroid 2–relatedfactor 2 (NRF2) is a master regulator of the antioxidant responsepathway and an attractive target for treating diseases driven by oxidativestress, such as peripheral neuropathy. While activation of NRF2 bymonomethyl fumarate (MMF) is well established, the systemic exposureand broad side-effect profile of MMF and its two FDA-approved prodrugs,diroximel fumarate and dimethyl fumarate, limit their broader therapeuticutility. To address this limitation, we present a series of α-ketoester-functionalized prodrugs of MMF (<strong>1–21</strong>), designedto release therapeutically active MMF selectively at the site of oxidativestress. These prodrugs were designed to exploit elevated pathologicallevels of reactive oxygen species (ROS), which trigger Baeyer–Villigeroxidation of the α-keto ester moiety, resulting in rapid hydrolysisof the generated anhydride and localized MMF release. Multiple α-ketoesters (<strong>1–11, 13–16</strong>, and <strong>18–21</strong>) demonstrated activity relative to MMF in our <em>in vitro</em> NRF2 reporter cell assay, but only in the presence of H₂O₂. Furthermore, structure–property relationship(SPR) analysis revealed that prodrugs with simple alkyl α-ketoesters demonstrated the highest levels of NRF2 activation and therapeuticefficacy. Specifically, α-keto esters <strong>4</strong>, <strong>5</strong>, and <strong>6</strong>, functionalized with trideutero methyl,ethyl, and iso-propyl esters, respectively, exhibit strong tissue-specificNRF2 activation <em>in vivo</em>, where <strong>4</strong> demonstratedfull reversal of mechanical allodynia in a mouse model of neuropathy.These findings firmly establish α-keto ester prodrugs of MMFas a next-generation NRF2-targeting modality that overcomes the systemicexposure and off-target liabilities of existing fumarate therapiesby exploiting pathological ROS as a trigger.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2961–2970"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148402915","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}

{"title":"Kynurenic Acid, a Key Endogenous Neuroprotective Agent: Role of Its Derivatives in Therapeutics","authors":"Swati Verma,&nbsp;Ramesh Ambatwar,&nbsp;Ashok Kumar Datusalia,&nbsp;Gopal L. Khatik","doi":"10.1021/acschemneuro.6c00081","DOIUrl":"10.1021/acschemneuro.6c00081","url":null,"abstract":"<p>Kynurenic acid (KYNA) is an endogenous molecule thatacts as anonselective antagonist of ionotropic glutamate receptors and hasbeen shown to have neuroprotective properties. Although KYNA has shownconsiderable therapeutic potential in neurodegenerative disorders,its limited permeability across the blood–brain barrier restrictsits direct clinical application. To overcome this limitation, variousester and amide derivatives have been developed as prodrugs to enhancebrain delivery and subsequently release KYNA within the central nervoussystem. Beyond serving as prodrugs, KYNA derivatives have attractedsubstantial interest in medicinal chemistry due to their ability tointeract with multiple molecular targets. Additionally, these compoundsexhibit a wide range of biological activities, including potentialtreatments for Alzheimer’s disease, Parkinson’s disease,Huntington’s disease, and psychiatric disorders. Therefore,kynurenic acid-based scaffolds have prompted further research intotheir derivatives, leading to a range of structurally distinct products.Here, we discuss the neuroprotective role of KYNA and its derivatives,which exhibit diverse bioactivities.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2775–2801"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148395408","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}

{"title":"Development of Aryl Cyano Amides for Fluorescence Discrimination of Tau and Amyloid Beta Deposits in Tissue","authors":"R. Erin Jessup,&nbsp;Rachel S. Ehrlich,&nbsp;Kristine L. Teppang,&nbsp;Saswata Dasgupta,&nbsp;Christina J. Sigurdson,&nbsp;Jerry Yang","doi":"10.1021/acschemneuro.6c00316","DOIUrl":"10.1021/acschemneuro.6c00316","url":null,"abstract":"<p>The accumulation of amyloid aggregatessuch as amyloid beta (Aβ)and tau deposits in the brain is a hallmark of many neurodegenerativediseases including Alzheimer’s disease. Recent advances inoptical imaging have shown that fluorescent probes can detect amyloidsin living patients, potentially aiding in diagnosis. Here, we investigatestructural modifications of amyloid-targeting Aryl Cyano Amide-basedfluorophores aimed at enhancing their ability to discriminate betweendifferent amyloid aggregates, such as Aβ and tau. We identifytwo structural parameters that synergistically enable increased sensitivityto environmental polarity, which makes it possible to discriminatethese amyloids through inspection of the color of fluorescence emission.This colorimetric discrimination can provide detailed informationon amyloid composition and could expand the use of fluorescence imagingfor diagnosis and monitoring of neurodegenerative diseases.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2910–2917"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148519531","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}

{"title":"Proliferative Effects of the Psychedelic N,N-Dimethyltryptamine (DMT) in Human Neural Stem Cells","authors":"José Alexandre Salerno,&nbsp;Elizabeth R. Dominguez,&nbsp;Karina Karmirian,&nbsp;Breno A.B.M.S. Arrais,&nbsp;Juliano Alves,&nbsp;Giovanna Erjautz,&nbsp;Kennedy Kroening,&nbsp;Leticia R. Q. Souza,&nbsp;Isis Ornelas,&nbsp;Stevens Rehen","doi":"10.1021/acschemneuro.6c00209","DOIUrl":"10.1021/acschemneuro.6c00209","url":null,"abstract":"<p>The serotonergic psychedelic <em>N,N</em>-dimethyltryptamine(DMT) produces rapid antidepressant effects in preclinical and earlyclinical studies. Therapeutic benefits have been linked to sustainedneural plasticity, including adult neurogenesis in rodents. Whetherbrief DMT exposure engages proliferative responses in human neuralstem cells (NSCs) remains unresolved. Using human iPSC-derived NSCs,we found that 24 h DMT treatment increased proliferation in a concentration-dependentmanner (half-maximal effect at 59.7 nM) and upregulated G1 cell-cycleregulators. DMT also shifted trophic gene expression, decreasing neurotrophin-3while increasing nerve growth factor and brain-derived neurotrophicfactor (BDNF) transcripts and intracellular BDNF protein. After washout,DMT-primed NSCs formed larger neurospheres, with progenitor and earlyneuronal marker composition matching controls by day 10. These findingsdemonstrate that brief DMT exposure is sufficient to engage proliferativeand neurotrophin-associated responses in human NSCs at concentrationsconsistent with those reported for DMT-induced plasticity across othersystems.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2901–2909"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148416920","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}

{"title":"PCSK9 as an Emerging Target for Cerebrovascular Dysfunction and Neuroinflammation in Ischemic Stroke","authors":"Carolina M. Vela,&nbsp;Josephin Wagner,&nbsp;Pal Pacher,&nbsp;Falk W. Lohoff","doi":"10.1021/acschemneuro.6c00171","DOIUrl":"10.1021/acschemneuro.6c00171","url":null,"abstract":"<p>Cerebrovasculardisease is a leading cause of death andlong-termdisability worldwide, most commonly manifesting as ischemic stroke.The pathogenesis of ischemic stroke is largely driven by atheroscleroticdiseases of the cerebral and extracranial vasculature, where lipidaccumulation and vascular inflammation play central roles. Proproteinconvertase subtilisin/kexin type 9 (PCSK9) is a key mediator in thisprocess. Elevated circulating PCSK9 contributes to stroke risk andseverity across multiple stages of disease progression, promotingatherogenesis, plaque instability, and thrombosis. It exacerbatesacute ischemic injury by elevating circulating low-density lipoproteincholesterol (LDL-C) and promoting vascular inflammation via upregulationof monocyte adhesion, foam cell formation, and cytokine release. Followingcerebral ischemia, upregulated PCSK9 also contributes to neuroinflammationwithin the brain parenchyma, thereby driving secondary neuronal injuryand poor neurological outcomes. Preclinical stroke models have shownthat PCSK9 inhibition (PCSK9i) is effective within this neurovascularcontext, attenuating both vascular and neuroinflammatory signalingand thereby limiting ischemic injury. Recent clinical trials havefocused on the potential of PCSK9i for broader cardiometabolic indicationsand stroke prevention, drawing on evidence that treatment can reducethe risk of these events and improve neurological outcomes for patients.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2818–2822"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148409718","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}