Neurochemistry international最新文献

{"title":"The protective effects of EGCG was associated with HO-1 active and microglia pyroptosis inhibition in experimental intracerebral hemorrhage","authors":"Bing Bao ,&nbsp;Xiao-Ping Yin ,&nbsp;Xiao-Qing Wen ,&nbsp;Yi-Jun Suo ,&nbsp;Zhi-Ying Chen ,&nbsp;Dong -Ling Li ,&nbsp;Qin Lai ,&nbsp;Xian-Ming Cao ,&nbsp;Qiu-Min Qu","doi":"10.1016/j.neuint.2023.105603","DOIUrl":"10.1016/j.neuint.2023.105603","url":null,"abstract":"<div><p><span><span><span>Intracerebral hemorrhage (ICH), which has high mortality and disability rate is associated with microglial </span>pyroptosis and </span>neuroinflammation, and the effective treatment methods are limited Epigallocatechin-3-gallate (EGCG) has been found to play a cytoprotective role by regulating the anti-inflammatory response to pyroptosis in other </span>systemic diseases<span><span>. However, the role of EGCG in microglial pyroptosis and neuroinflammation after ICH remains unclear. In this study, we investigated the effects of EGCG pretreatment on neuroinflammation-mediated neuronal pyroptosis and the underlying </span>neuroprotective<span><span> mechanisms in experimental ICH. EGCG pretreatment was found to remarkably improved neurobehavioral performance, and decreased the hematoma<span> volume and cerebral edema in mice. We found that EGCG pretreatment attenuated the release of hemin-induced </span></span>inflammatory cytokines<span> (IL-1β, IL-18, and TNF-α). EGCG significantly upregulated the expression of heme oxygenase-1 (HO-1), and downregulated the levels of pyroptotic molecules and inflammatory cytokines including Caspase-1, GSDMD, NLRP3<span>, mature IL-1β, and IL-18. EGCG pretreatment also decreased the number of Caspase-1-positive microglia and GSDMD along with NLRP3-positive microglia after ICH. Conversely, an HO-1-specific inhibitor (ZnPP), significantly inhibited the anti-pyroptosis and anti-neuroinflammation effects of EGCG. Therefore, EGCG pretreatment alleviated microglial pyroptosis and neuroinflammation, at least in part through the Caspase-1/GSDMD/NLRP3 pathway by upregulating HO-1 expression after ICH. In addition, EGCG pretreatment promoted the polarization of microglia from the M1 phenotype to M2 phenotype after ICH. The results suggest that EGCG is a potential agent to attenuate neuroinflammation via its anti-pyroptosis effect after ICH.</span></span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105603"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187311","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":"Cell membrane-based nanomaterials for therapeutics of neurodegenerative diseases","authors":"Phuong-Trang Nguyen-Thi ,&nbsp;Thuy Trang Nguyen ,&nbsp;Hoang Long Phan ,&nbsp;Thanh-Tam Ho ,&nbsp;Toi Van Vo ,&nbsp;Giau Van Vo","doi":"10.1016/j.neuint.2023.105612","DOIUrl":"10.1016/j.neuint.2023.105612","url":null,"abstract":"<div><p><span>Central nervous system (CNS) diseases such as Alzheimer's disease<span> (AD), Parkinson's disease<span><span> (PD), glioblastoma (GBM), and </span>peripheral nerve injury have been documented as incurable diseases, which lead to serious impacts on human health especially prevalent in the aging population worldwide. Most of the treatment strategies fail due to low efficacy, toxicity, and poor brain penetration. Recently, advancements in nanotechnology have helped alleviate the challenges associated with the application of cell membrane-based </span></span></span>nanomaterials<span> against CNS diseases. In the following review, the existing types of cell membrane-based nanomaterials systems which have improved therapeutic efficacy for CNS diseases would be described. A summary of recent progress in the incorporation of nanomaterials in cell membrane-based production, separation, and analysis will be provided. Addition to, challenges relate to large-scale manufacturing of cell membrane-based nanomaterials and future clinical trial of such platforms will be discussed.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105612"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10260702","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":"PKR inhibitor protects spinal cord injury through mitigating endoplasmic reticulum stress and pyroptosis","authors":"Ze Yang ,&nbsp;Ming Sheng ,&nbsp;Meng Wang ,&nbsp;Long Cheng ,&nbsp;Xin Sun","doi":"10.1016/j.neuint.2023.105632","DOIUrl":"10.1016/j.neuint.2023.105632","url":null,"abstract":"<div><h3>Objectives</h3><p><span>The goal of the study was to reveal the regulatory role of protein kinase R (PKR) in </span>spinal cord injury<span> (SCI), a devasting disorder of the neurological system, and to elucidate its potential mechanism.</span></p></div><div><h3>Methods</h3><p><span><span>The established animal and cellular models of SCI were treated by the PKR inhibitor C12. Histological injury and tissue apoptosis were assessed via H&amp;E staining and </span>TUNEL assays<span>, respectively. Basso-Beattie-Bresnahan (BBB) scoring as well as forelimb grip strength tests were employed to evaluate functional recovery. The production of </span></span>ROS<span><span> and cytokines were appraised via their related commercial kits. Western blot<span> and immunofluorescence assay were used to examine protein expression. CCK-8 method was used to assay cell activity. Co-immunoprecipitation assay was conducted to measure the affinity of PKR with </span></span>STAT1.</span></p></div><div><h3>Results</h3><p><span>PKR expression was enhanced following SCI, and the PKR inhibitor C16 mitigated histological injury, cell apoptosis and water content in spinal cord, and improved function recovery following SCI. Meanwhile, C16 attenuated ER stress<span>, pyroptosis, NLRP3 </span></span>inflammasome and inflammation in mice with SCI and in BV-2 cells challenged with LPS. Additionally, PKR interacted with STAT1 in BV-2 cells, and STAT1 knockdown inhibited ER stress, pyroptosis and inflammation in BV-2 cells challenged with LPS. The protective role of C16 in BV-2 cells exposed to LPS were partly abolished by STAT1 overexpression.</p></div><div><h3>Conclusion</h3><p>PKR inhibition might be a prospective effective approach to attenuating SCI and accelerating function recovery through modulating microglial pyroptosis and ER stress.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"172 ","pages":"Article 105632"},"PeriodicalIF":4.2,"publicationDate":"2023-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49688116","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 effects of phenylalanine and tyrosine levels on dopamine production in rat PC12 cells. Implications for treatment of phenylketonuria, tyrosinemia type 1 and comorbid neurodevelopmental disorders","authors":"Peter D. Szigetvari ,&nbsp;Sudarshan Patil ,&nbsp;Even Birkeland ,&nbsp;Rune Kleppe ,&nbsp;Jan Haavik","doi":"10.1016/j.neuint.2023.105629","DOIUrl":"10.1016/j.neuint.2023.105629","url":null,"abstract":"<div><p>Phenylketonuria (PKU) is an autosomal recessive metabolic disorder caused by mutations in the phenylalanine hydroxylase (PAH) gene, resulting in phenylalanine accumulation and impaired tyrosine production. In Tyrosinemia type 1 (TYRSN1) mutations affect fumarylacetoacetate hydrolase, leading to accumulation of toxic intermediates of tyrosine catabolism. Treatment of TYRSN1 with nitisinone results in extreme tissue levels of tyrosine. Although PKU and TYRSN1 have opposite effects on tyrosine levels, both conditions have been associated with neuro-psychiatric symptoms typically present in ADHD, possibly indicating an impaired dopamine (DA) synthesis. However, concrete <em>in vivo</em> data on the possible molecular basis for disrupted DA production under disease mimicking conditions have been lacking. In pursuit to uncover associated molecular mechanisms, we exposed an established, DA producing cell line (PC12) to different concentrations of phenylalanine and tyrosine in culture media. We measured the effects on viability, proteomic composition, tyrosine, DA and tyrosine hydroxylase (TH) levels and TH phosphorylation. TH catalyzes the rate-limiting step in DA synthesis. High extracellular levels of phenylalanine depleted cells of intracellular tyrosine and DA. Compared to physiological levels (75 μM), either low (35 μM) or high concentrations of tyrosine (275 or 835 μM) decreased cellular DA, TH protein, and its phosphorylation levels. Using deep proteomic analysis, we identified multiple proteins, biological processes and pathways that were altered, including enzymes and transporters involved in amino acid metabolism. Using this information and published data, we developed a mathematical model to predict how extracellular levels of aromatic amino acids can affect the cellular synthesis of DA <em>via</em> different mechanisms. Together, these data provide new information about the normal regulation of neurotransmitter synthesis and how this may be altered in neurometabolic disorders, such as PKU and TYRSN1, with implications for the treatment of cognitive symptoms resulting from comorbid neurodevelopmental disorders.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"171 ","pages":"Article 105629"},"PeriodicalIF":4.2,"publicationDate":"2023-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0197018623001572/pdfft?md5=3af11bcf8e519511734ff91fda5704dc&pid=1-s2.0-S0197018623001572-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49672699","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}

{"title":"Mechanisms and treatments of chronic pain after traumatic brain injury","authors":"QiLiang Chen ,&nbsp;Vimala Bharadwaj ,&nbsp;Karen-Amanda Irvine ,&nbsp;J. David Clark","doi":"10.1016/j.neuint.2023.105630","DOIUrl":"10.1016/j.neuint.2023.105630","url":null,"abstract":"<div><p><span>While pain after trauma generally resolves, some trauma patients experience pain for months to years after injury. An example, relevant to both combat and civilian settings, is chronic pain after traumatic brain injury<span> (TBI). Headache as well as pain in the back and extremities are common locations for TBI-related chronic pain to be experienced. TBI-related pain can exist alone or can exacerbate pain from other injuries long after healing has occurred. Consequences of chronic pain in these settings include increased suffering, higher levels of disability, serious emotional problems, and worsened cognitive deficits. The current review will examine recent evidence regarding dysfunction of endogenous pain modulatory mechanisms, neuroplastic changes in the trigeminal circuitry and alterations in spinal nociceptive processing as contributors to TBI-related chronic pain. Key pain modulatory centers including the </span></span>locus coeruleus<span>, periaqueductal grey<span><span> matter, and rostroventromedial medulla are vulnerable to TBI. Both the rationales and existing evidence for the use of monoamine reuptake inhibitors<span>, CGRP antagonists, CXCR2 </span></span>chemokine<span> receptor antagonists, and interventional therapies will be presented. While consensus guidelines for the management of chronic post-traumatic TBI-related pain are lacking, several approaches to this clinically challenging situation deserve focused evaluation and may prove to be viable therapeutic options.</span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"171 ","pages":"Article 105630"},"PeriodicalIF":4.2,"publicationDate":"2023-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49672698","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":"Disturbance of mitochondrial functions caused by N-acetylglutamate and N-acetylmethionine in brain of adolescent rats: Potential relevance in aminoacylase 1 deficiency","authors":"Vanessa Trindade Bortoluzzi ,&nbsp;Rafael Teixeira Ribeiro ,&nbsp;Ângela Beatris Zemniaçak ,&nbsp;Sâmela de Azevedo Cunha ,&nbsp;Jörn Oliver Sass ,&nbsp;Roger Frigério Castilho ,&nbsp;Alexandre Umpierrez Amaral ,&nbsp;Moacir Wajner","doi":"10.1016/j.neuint.2023.105631","DOIUrl":"10.1016/j.neuint.2023.105631","url":null,"abstract":"<div><p><span>Aminoacylase 1 (ACY1) deficiency is a rare genetic disorder that affects the breakdown of short-chain aliphatic </span><em>N</em><span><span>-acetylated amino acids<span><span>, leading to the accumulation of these amino acid derivatives in the urine of patients. Some of the affected individuals have presented with heterogeneous neurological symptoms such as psychomotor delay, seizures, and </span>intellectual disability. Considering that the pathological mechanisms of </span></span>brain damage in this disorder remain mostly unknown, here we investigated whether major metabolites accumulating in ACY1 deficiency, namely </span><em>N</em>-acetylglutamate (NAG) and <em>N</em>-acetylmethionine (NAM), could be toxic to the brain by examining their in vitro effects on important mitochondrial properties. We assessed the effects of NAG and NAM on membrane potential, swelling, reducing equivalents, and Ca²⁺<span> retention capacity in purified mitochondrial preparations obtained from the brain of adolescent rats. NAG and NAM decreased mitochondrial membrane potential, reducing equivalents, and calcium retention capacity, and induced swelling in Ca</span>²⁺<span><span><span><span>-loaded brain mitochondria supported by glutamate plus </span>malate<span>. Notably, these changes were completely prevented by the classical inhibitors of mitochondrial permeability transition (MPT) pore cyclosporin A plus ADP and by </span></span>ruthenium red, implying the participation of </span>MPT and Ca</span>²⁺<span> in these effects. Our findings suggest that NAG- and NAM-induced disruption of mitochondrial functions involving MPT may represent relevant mechanisms of neuropathology in ACY1 deficiency.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"171 ","pages":"Article 105631"},"PeriodicalIF":4.2,"publicationDate":"2023-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49672697","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":"Stable isotope tracing reveals disturbed cellular energy and glutamate metabolism in hippocampal slices of aged male mice","authors":"Laura Mikél McNair,&nbsp;Jens Velde Andersen,&nbsp;Helle Sønderby Waagepetersen","doi":"10.1016/j.neuint.2023.105626","DOIUrl":"10.1016/j.neuint.2023.105626","url":null,"abstract":"<div><p>Neurons and astrocytes work in close metabolic collaboration, linking neurotransmission to brain energy and neurotransmitter metabolism. Dysregulated energy metabolism is a hallmark of the aging brain and may underlie the progressive age-dependent cognitive decline. However, astrocyte and neurotransmitter metabolism remains understudied in aging brain research. In particular, how aging affects metabolism of glutamate, being the primary excitatory neurotransmitter, is still poorly understood. Here we investigated critical aspects of cellular energy metabolism in the aging male mouse hippocampus using stable isotope tracing <em>in vitro</em>. Metabolism of [U–¹³C]glucose demonstrated an elevated glycolytic capacity of aged hippocampal slices, whereas oxidative [U–¹³C]glucose metabolism in the TCA cycle was significantly reduced with aging. In addition, metabolism of [1,2–¹³C]acetate, reflecting astrocyte energy metabolism, was likewise reduced in the hippocampal slices of old mice. In contrast, uptake and subsequent metabolism of [U–¹³C]glutamate was elevated, suggesting increased capacity for cellular glutamate handling with aging. Finally, metabolism of [¹⁵N]glutamate was maintained in the aged slices, demonstrating sustained glutamate nitrogen metabolism. Collectively, this study reveals fundamental alterations in cellular energy and neurotransmitter metabolism in the aging brain, which may contribute to age-related hippocampal deficits.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"171 ","pages":"Article 105626"},"PeriodicalIF":4.2,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0197018623001547/pdfft?md5=d366e106edf34772f7a86e79c0c1d838&pid=1-s2.0-S0197018623001547-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187313","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}

{"title":"Epigenetic modification impacting brain functions: Effects of physical activity, micronutrients, caffeine, toxins, and addictive substances","authors":"Rahul Mallick ,&nbsp;Asim K. Duttaroy","doi":"10.1016/j.neuint.2023.105627","DOIUrl":"10.1016/j.neuint.2023.105627","url":null,"abstract":"<div><p>Changes in gene expression are involved in many brain functions. Epigenetic processes modulate gene expression by histone modification and DNA methylation or RNA-mediated processes, which is important for brain function. Consequently, epigenetic changes are also a part of brain diseases such as mental illness and addiction. Understanding the role of different factors on the brain epigenome may help us understand the function of the brain. This review discussed the effects of caffeine, lipids, addictive substances, physical activity, and pollutants on the epigenetic changes in the brain and their modulatory effects on brain function.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"171 ","pages":"Article 105627"},"PeriodicalIF":4.2,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0197018623001559/pdfft?md5=5e56433843f9dc5b7172595b906b7019&pid=1-s2.0-S0197018623001559-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187312","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}

{"title":"DJ-1 inhibits ferroptosis in cerebral ischemia-reperfusion via ATF4/HSPA5 pathway","authors":"Yumei Li ,&nbsp;Tianyi Chen ,&nbsp;Ying Xue ,&nbsp;Yuan Wang ,&nbsp;Li Peng ,&nbsp;Chenglong Wang ,&nbsp;Shanshan Yu","doi":"10.1016/j.neuint.2023.105628","DOIUrl":"10.1016/j.neuint.2023.105628","url":null,"abstract":"<div><p><span><span>DJ-1 has been confirmed to have neuroprotective<span> effects. Ferroptosis is an iron-dependent </span></span>programmed cell death mode associated with </span>ischemic stroke<span>. The ATF4/HSPA5 pathway has been shown to play an important role in the regulation of ferroptosis. To explore the role and possible mechanism of DJ-1 in regulating ferroptosis in cerebral ischemia-reperfusion injury. In this study, Middle cerebral artery<span><span> occlusion/reperfusion (MCAO/R) was used to simulate cerebral ischemia-reperfusion injury in vivo. Detected ferroptosis-related indicators and observed mitochondrial morphology in brain tissue using transmission electron microscopy<span>. ATF4 was subsequently interfered to observe the effect of DJ-1 on ferroptosis. The results suggest that after interfering with DJ-1, the iron content and </span></span>malondialdehyde (MDA) content of ferroptosis-related indicators increased, the GSH content decreased, and the mitochondrial structure was severely damaged. We then found that DJ-1 attenuated ferroptosis following ATF4 reduction. In this study, we found that the neuroprotective effect of DJ-1 is related to the inhibition of ferroptosis, and its molecular mechanism is closely related to the ATF4/HSPA5 pathway, which may play a key role in inhibiting brain ischemia-reperfusion (I/R) ferroptosis.</span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"171 ","pages":"Article 105628"},"PeriodicalIF":4.2,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187314","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":"Comprehensive analysis of sex differences in the function and ultrastructure of hippocampal presynaptic terminals","authors":"Sung Rae Kim ,&nbsp;Yunkyung Eom ,&nbsp;Sung Hoon Lee","doi":"10.1016/j.neuint.2023.105570","DOIUrl":"10.1016/j.neuint.2023.105570","url":null,"abstract":"<div><p><span><span><span>Sex differences in the brain, encompassing variations in specific brain structures, size, cognitive function, and synaptic connections, have been identified across numerous species. While previous research has explored sex differences in postsynaptic structures, </span>synaptic plasticity, and hippocampus-dependent functions, the hippocampal </span>presynaptic terminals<span><span><span><span> remain largely uninvestigated. The hippocampus is a critical structure responsible for multiple brain functions. This study examined presynaptic differences in </span>cultured hippocampal neurons derived from male and female mice using a combination of biochemical assays, functional analyses measuring exocytosis and </span>endocytosis of </span>synaptic vesicle<span> proteins, ultrastructural analyses via electron microscopy, and presynaptic Ca</span></span></span>²⁺<span>-specific optical probes. Our findings revealed that female neurons exhibited a higher number of synaptic vesicles at presynaptic terminals compared to male neurons. However, no significant differences were observed in presynaptic protein expression, presynaptic terminal ultrastructure, synaptic vesicle exocytosis and endocytosis, or presynaptic Ca</span>²⁺ alterations between male and female neurons.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"169 ","pages":"Article 105570"},"PeriodicalIF":4.2,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10092511","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}