Journal of Neurochemistry最新文献

{"title":"The Role of Glial Cell Senescence in Alzheimer's Disease","authors":"Fadhl Alshaebi,&nbsp;Alessia Sciortino,&nbsp;Rakez Kayed","doi":"10.1111/jnc.70051","DOIUrl":"https://doi.org/10.1111/jnc.70051","url":null,"abstract":"<p>Glial cell senescence, characterized by the irreversible arrest of cell division and a pro-inflammatory secretory phenotype, has emerged as a critical player in the pathogenesis of Alzheimer's disease (<span>ad</span>). While much attention has been devoted to the role of neurons in <span>ad</span>, growing evidence suggests that glial cells, including astrocytes, microglia, and oligodendrocytes, contribute significantly to disease progression through senescence. In this review, we explore the molecular mechanisms underlying glial cell senescence in <span>ad</span>, focusing on the cellular signaling pathways, including DNA damage response and the accumulation of senescence-associated secretory phenotypes (SASP). We also examine how senescent glial cells exacerbate neuroinflammation, disrupt synaptic function, and promote neuronal death in <span>ad</span>. Moreover, we discuss emerging therapeutic strategies aimed at targeting glial cell senescence to mitigate the neurodegenerative processes in <span>ad</span>. By providing a comprehensive overview of current research on glial cell senescence in Alzheimer's disease, this review highlights its potential as a novel therapeutic target in the fight against <span>ad</span>.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690227","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":"Lipid Composition Diversity of the Human Brain White Matter Tracts","authors":"Marina Zavolskova,&nbsp;Dmitry Senko,&nbsp;Maria Osetrova,&nbsp;Olga Efimova,&nbsp;Elena Stekolshchikova,&nbsp;Gleb Vladimirov,&nbsp;Evgeny Nikolaev,&nbsp;Philipp Khaitovich","doi":"10.1111/jnc.70042","DOIUrl":"https://doi.org/10.1111/jnc.70042","url":null,"abstract":"<div>\u0000 \u0000 <p>Understanding the molecular basis of the structural organization of the human brain may shed light on its functional mechanism. We present spatial lipidomics analysis of human brain sections containing neocortical gray matter and two white matter regions representing two axonal tracks: <i>the cingulum bundle</i> and <i>the corpus callosum</i>. Using matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) we identify lipid composition differences not only between gray and white matter but also between two axonal tracks. Results, obtained with the MALDI-MSI method, correlated with ultra-performance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS) analysis of these brain regions, with Spearman's correlation coefficient equal to 0.48 (the cingulum bundle vs. gray matter), 0.47 (the corpus callosum vs. gray matter), 0.33 (the cingulum bundle vs. the corpos callosum) on 75 lipids annotated in both experiments. Using UPLC-MS/MS analysis, we further identified specific lipid classes that distinguished the two white matter regions (CL, PG, LPE), while gray and white matter comparison yielded well-established differences in lipid composition between myelin-rich and myelin poor regions (CL, DG, Cholesterol). Our findings highlight the significance of in-depth molecular analysis of brain regions and enhance our comprehension of the brain's molecular composition.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689743","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":"Regulation of CNS Lipids by Protease Activated Receptor 1","authors":"Hyesook Yoon,&nbsp;Erin M. Triplet,&nbsp;Lincoln Wurtz,&nbsp;Whitney L. Simon,&nbsp;Chan-Il Choi,&nbsp;Isobel A. Scarisbrick","doi":"10.1111/jnc.70047","DOIUrl":"https://doi.org/10.1111/jnc.70047","url":null,"abstract":"<div>\u0000 \u0000 <p>Disruptions in the metabolism of cholesterol and other lipids are strongly implicated in the pathogenesis of neurological disease. The CNS is highly enriched in cholesterol, which is primarily synthesized <i>de novo</i>. Cholesterol synthesis is also rate limiting for myelin regeneration. Given that knockout of the thrombin receptor (Protease Activated Receptor 1 (PAR1)) accelerates myelin regeneration, here we sought to determine the potential regulatory actions of PAR1 in CNS cholesterol and lipid metabolism in the intact adult CNS and during myelin regeneration. We present quantitative PCR and RNAseq evidence from murine spinal cords at the peak of myelination and in adulthood showing PAR1 knockout is associated with increased gene expression for cholesterol biosynthesis (Hmgcs1, Hmgcr, Sqle, and Dhcr7), lipid transport (ApoE, Abca1, and Ldlr), and intracellular processing (Lcat, Npc1, and Npc2) at one or more time points examined. An upregulation of genes involved in the synthesis of other lipids enriched in the myelin membrane, specifically Fa2h, Ugt8a, and Gal3st1, was also observed in PAR1 knockouts. Transcription factors essential for lipid and cholesterol production (Srebf1 and Srebf2) were also increased in PAR1 knockout spinal cords at the postnatal day 21 peak of myelination and at day 45. GC–MS and LC–MS quantification of lipids demonstrated coordinate increases in the abundance of select cholesterol and lipid species in the spinal cords of PAR1 knockout mice, including enrichment of esterified cholesterol, together with sphingomyelins and sphingolipids. Co-localization of the SREBP1 and SREBP2 transcription factors, as well as HMGCS1, a rate-limiting enzyme in cholesterol biosynthesis, to glia during remyelination post-lysolecithin or cuprizone-mediated demyelination showed a prominent regulatory role for PAR1 in Olig2+ oligodendrocytes. PAR1 knockouts also demonstrated elevated levels of SREBP2 in more mature GST3+ oligodendrocytes and SREBP1 in GFAP+ astrocytes during remyelination post-lysolecithin. These findings demonstrate novel roles for PAR1 as a regulator of CNS cholesterol and lipid metabolism and its potential as a therapeutic target to increase cholesterol availability to improve myelin regeneration.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689677","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":"Hippocampal Inhibitory Interneuron-Specific DREADDs Treatment Alters mTORC1-4E-BP Signaling and Impairs Memory Formation","authors":"Ziying Huang,&nbsp;Niaz Mahmood,&nbsp;Jean-Claude Lacaille,&nbsp;Shane Wiebe,&nbsp;Nahum Sonenberg","doi":"10.1111/jnc.70048","DOIUrl":"https://doi.org/10.1111/jnc.70048","url":null,"abstract":"<p>Control of protein synthesis via the mechanistic target of rapamycin complex 1 (mTORC1) is essential for learning and memory. However, the cell-type-specific and spatiotemporal regulation of this pathway during memory formation is not well understood. In this study, we expressed artificial human muscarinic M3 [hM3D(Gq)] or M4 [hM4D(Gi)] designer receptors exclusively activated by designer drugs (DREADDs) in hippocampal CA1 excitatory or inhibitory neurons of adult mice. We studied the impact of clozapine-N-oxide (CNO), a synthetic DREADDs agonist, on the mTORC1 pathway and long-term memory. hM3D(Gq) and hM4D(Gi) activate or inactivate, respectively, mTORC1 signaling in hippocampal interneurons, as indicated by the phosphorylation of its targets, eukaryotic initiation factor 4E-binding proteins (4E-BP1/2) and ribosomal protein S6 (S6). Activation of either hM3D(Gq) or hM4D(Gi) in mice immediately after training in memory tasks impaired long-term memory formation in inhibitory, but not in excitatory neurons. The findings underscore the importance of activity-dependent mTORC1–4E-BP1/2 signaling in hippocampal inhibitory interneurons for memory formation.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689740","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":"Input-Specific Localization of NMDA Receptor GluN2 Subunits in Thalamocortical Neurons","authors":"Mackenzie A. Topolski,&nbsp;Brian L. Gilmore,&nbsp;Rabeya Khondaker,&nbsp;Juliana A. Michniak,&nbsp;Carleigh Studtmann,&nbsp;Yang Chen,&nbsp;Gwen N. Wagner,&nbsp;Aaron E. Pozo-Aranda,&nbsp;Shannon Farris,&nbsp;Sharon A. Swanger","doi":"10.1111/jnc.70049","DOIUrl":"https://doi.org/10.1111/jnc.70049","url":null,"abstract":"<p>Molecular and functional diversity among synapses is generated, in part, by differential expression of neurotransmitter receptors and their associated protein complexes. <i>N</i>-methyl-<i>D</i>-aspartate receptors (NMDARs) are tetrameric ionotropic glutamate receptors that most often comprise two GluN1 and two GluN2 subunits. NMDARs generate functionally diverse synapses across neuron populations through cell-type-specific expression patterns of GluN2 subunits (GluN2A–2D), which have vastly different functional properties and distinct downstream signaling. Diverse NMDAR function has also been observed at anatomically distinct inputs to a single neuron population. However, the mechanisms that generate input-specific NMDAR function remain unknown, as few studies have investigated subcellular GluN2 subunit localization in native brain tissue. We investigated NMDAR synaptic localization in thalamocortical (TC) neurons expressing all four GluN2 subunits. Utilizing high-resolution fluorescence imaging and knockout-validated antibodies, we revealed subtype- and input-specific GluN2 localization at corticothalamic (CT) versus sensory inputs to TC neurons in 4-week-old male and female C57Bl/6J mice. GluN2B was the most abundant postsynaptic subunit across all glutamatergic synapses, followed by GluN2A and GluN2C, and GluN2D was localized to the fewest synapses. GluN2B was preferentially localized to CT synapses over sensory synapses, while GluN2A and GluN2C were more abundant at sensory inputs compared to CT inputs. Furthermore, postsynaptic scaffolding proteins PSD-95 and SAP102 were preferentially colocalized with specific GluN2 subunits, and SAP102 was more abundant at sensory synapses than PSD-95. This work indicates that TC neurons exhibit subtype- and input-specific localization of diverse NMDARs and associated scaffolding proteins that likely contribute to functional differences between CT and sensory synapses.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689742","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":"Dynamics of Neuronal and Astrocytic Energy Molecules in Epilepsy","authors":"Kota Furukawa,&nbsp;Yoko Ikoma,&nbsp;Yusuke Niino,&nbsp;Yuichi Hiraoka,&nbsp;Kohichi Tanaka,&nbsp;Atsushi Miyawaki,&nbsp;Johannes Hirrlinger,&nbsp;Ko Matsui","doi":"10.1111/jnc.70044","DOIUrl":"10.1111/jnc.70044","url":null,"abstract":"<p>The dynamics of energy molecules in the mouse brain during metabolic challenges induced by epileptic seizures were examined. A transgenic mouse line expressing a fluorescence resonance energy transfer (FRET)-based adenosine triphosphate (ATP) sensor, selectively expressed in the cytosol of neurons, was used. An optical fiber was inserted into the hippocampus, and changes in cytosolic ATP concentration were estimated using the fiber photometry method. To induce epileptic neuronal hyperactivity, a train of electrical stimuli was delivered to a bipolar electrode placed alongside the optical fiber. Although maintaining a steady cytosolic ATP concentration is crucial for cell survival, a single episode of epileptic neuronal hyperactivity drastically reduced neuronal ATP levels. Interestingly, the magnitude of ATP reduction did not increase with the exacerbation of epilepsy, but rather decreased. This suggests that the primary consumption of ATP during epileptic neuronal hyperactivity may not be solely directed toward restoring the Na⁺ and K⁺ ionic imbalance caused by action potential bursts. Cytosolic ATP concentration reflects the balance between supply and consumption. To investigate the metabolic flux leading to neuronal ATP production, a new FRET-based pyruvate sensor was developed and selectively expressed in the cytosol of astrocytes in transgenic mice. Upon epileptic neuronal hyperactivity, an increase in astrocytic pyruvate concentration was observed. Changes in the supply of energy molecules, such as glucose and oxygen, due to blood vessel constriction or dilation, as well as metabolic alterations in astrocyte function, may contribute to cytosolic ATP dynamics in neurons.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663709","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":"The Evolution of Experimental Rodent Models for Prion Diseases","authors":"Joseph P. DeFranco,&nbsp;Glenn C. Telling","doi":"10.1111/jnc.70039","DOIUrl":"10.1111/jnc.70039","url":null,"abstract":"<p>Prion diseases are a group of fatal, neurodegenerative diseases that affect animals and humans. These diseases are characterized by the conformational conversion of normal, host-encoded PrP^C into a disease-causing prion isoform, PrP^Sc. Significant advancements in biological, genetic, and prion research have led to the capability of studying this pathogenetic process using recombinant proteins, ex vivo systems, in vitro models, and mammalian hosts, the latter being the gold standard for assaying prion infectivity, transmission, and strain evolution. While devoid of nucleic acid, prions encipher strain information by the conformation of their constituent infectious proteins, with diversity altering pathogenesis, host-range dynamics, and the efficacy of therapeutics. To properly study the strain properties of natural prions and develop appropriate therapeutic strategies, it is essential to utilize models that authentically recapitulate these infectious agents in experimental mammalian hosts. In this review, we examine the evolution of research on prion diseases using non-transgenic and transgenic animals, primarily focusing on rodent models. We discuss the successes and limitations of each experimental system and provide insights based on recent findings in novel gene-targeted mice.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663700","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":"Metal Dyshomeostasis as a Driver of Gut Pathology in Autism Spectrum Disorders","authors":"Katelyn O'Grady,&nbsp;Andreas M. Grabrucker","doi":"10.1111/jnc.70041","DOIUrl":"10.1111/jnc.70041","url":null,"abstract":"<p>Despite being classified as neurodevelopmental disorders, in recent years, there has been a growing interest in the association between autism spectrum disorders (ASDs) and gut pathology. This comprehensive and systematic review explores a potential mechanism underlying gut pathology in ASDs, including alterations in gut microbiota, intestinal permeability, immune dysregulation, and gastrointestinal (GI) symptoms. Specifically, it delves into the role of toxic and essential metals and their interplay, affecting the development and function of the GI tract. The review also discusses the potential implications of this gut pathology in the development and management of ASDs. Studies have shown that heavy metal exposure, whether through environmental sources or dietary intake, can disrupt the delicate balance of trace elements in the gut. This disruption can adversely affect zinc homeostasis, potentially exacerbating gut pathology in individuals with ASDs. The impaired zinc absorption resulting from heavy metal exposure may contribute to the immune dysregulation, oxidative stress, and inflammation observed in the gut of individuals with ASDs. By shedding light on the multifaceted nature of gut pathology, including the impact of metal dyshomeostasis as a non-genetic factor in ASD, this review underscores the significance of the gut-brain axis in the etiology and management of ASDs.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663716","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":"Cannabidiol Protects Against Neurotoxic Reactive Astrocytes-Induced Neuronal Death in Mouse Model of Epilepsy","authors":"Haojie Ye,&nbsp;Yuhui Wan,&nbsp;Xin Wang,&nbsp;Suji Wang,&nbsp;Xiansen Zhao,&nbsp;Xinshi Wang,&nbsp;Tianfu Yu,&nbsp;Chao Yan,&nbsp;Xin Tian,&nbsp;Zhang-Peng Chen,&nbsp;Xiangyu Liu","doi":"10.1111/jnc.70038","DOIUrl":"https://doi.org/10.1111/jnc.70038","url":null,"abstract":"<div>\u0000 \u0000 <p>Reactive astrocytes play a critical role in the initiation and progression of epilepsy, but their molecular subtypes and functional characterization are not fully understood. In this study, we report the existence of neurotoxic reactive astrocytes, a recently identified subtype, that contribute to neuronal death in the epileptic brain. In a kainic acid (KA)-induced mouse model of epilepsy, we show that neurotoxic reactive astrocytes are induced by microglia-secreted cytokines, including IL-1α, TNFα, and C1q, and are detectable as early as 7 days post-KA stimulation. These cells exhibit a distinct molecular signature marked by elevated expression of complement 3 and adenosine 2A receptor. Transcriptomics and metabolomics analyses of human brain tissues from temporal lobe epilepsy (TLE) patients and an epileptic mouse model reveal that neurotoxic reactive astrocytes induce neuronal damage through lipid-related mechanisms. Moreover, our results demonstrate that the anti-seizure medication cannabidiol (CBD) and an adenosine 2A receptor antagonist can both suppress the formation of neurotoxic reactive astrocytes, mitigate gliosis, and reduce neuronal loss in a mouse model of epilepsy. Electrophysiological and behavioral studies indicate that cannabidiol attenuates seizure symptoms and enhances memory capabilities in epileptic mice. Our findings suggest that neurotoxic reactive astrocytes are formed at an early stage in both the KA-induced mouse model of epilepsy and TLE patients and can contribute to neuronal loss through releasing toxic lipids. Importantly, cannabidiol emerges as a promising therapeutic drug for targeted intervention against neurotoxic reactive astrocytes in adult epilepsy.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143638986","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":"Correction to “Inhalation of Hydrogen Gas Mitigates Sevoflurane-Induced Neuronal Apoptosis in the Neonatal Cortex and is Associated With Changes in Protein Phosphorylation”","authors":"","doi":"10.1111/jnc.70040","DOIUrl":"https://doi.org/10.1111/jnc.70040","url":null,"abstract":"<p>\u0000 <span>Iketani, M.</span>, <span>Hatomi, M.</span>, <span>Fujita, Y.</span>, <span>Watanabe, N.</span>, <span>Ito, M.</span>, <span>Kawaguchi, H.</span>, &amp; <span>Ohsawa, I.</span> (<span>2024</span>). <span>Inhalation of hydrogen gas mitigates sevoflurane-induced neuronal apoptosis in the neonatal cortex and is associated with changes in protein phosphorylation</span>. <i>Journal of Neurochemistry</i>, <span>168</span>, <span>2775</span>–<span>2790</span>. https://doi.org/10.1111/jnc.16142\u0000 </p><p>In the paper by Iketani et al. (2024), there were some typographical errors, where Greek letters have been mistakenly replaced with Latin letters.</p><p>In Section 3.3, the text “The measured concentrations were around 15 mM, which is very similar to the concentration at which 2% H₂ gas dissolves in water, that is, 15.6 mM. Conversely, the concentration of H₂ was much lower in mice whose bodies were exposed to 2% H₂ gas only from the neck downwards: ca. 3 mM”.</p><p>The text should read “The measured concentrations were around 15 μM, which is very similar to the concentration at which 2% H₂ gas dissolves in water, that is, 15.6 μM. Conversely, the concentration of H₂ was much lower in mice whose bodies were exposed to 2% H₂ gas only from the neck downwards: ca. 3 μM.”</p><p>In Figure 3b, the units on the y-axis were incorrect. It should have read ‘concentration (μM). The correct figure is shown below.</p><p>We apologize for these errors.</p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595412","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}