Frontiers in Cellular Neuroscience最新文献

{"title":"Editorial: Paradigm shifts and innovations in cellular neuroscience.","authors":"Enrico Cherubini, Arianna Maffei, Egidio D'Angelo, Dirk M Hermann, Marie-Ève Tremblay, Christian Hansel","doi":"10.3389/fncel.2025.1644329","DOIUrl":"10.3389/fncel.2025.1644329","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1644329"},"PeriodicalIF":4.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12301337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144729287","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":"Chronic benzodiazepine treatment triggers gephyrin scaffold destabilization and GABA_AR subsynaptic reorganization.","authors":"Caitlyn A Chapman, Nadya Povysheva, Tyler B Tarr, Jessica L Nuwer, Stephen D Meriney, Jon W Johnson, Tija C Jacob","doi":"10.3389/fncel.2025.1624813","DOIUrl":"10.3389/fncel.2025.1624813","url":null,"abstract":"<p><p>Benzodiazepines (BZDs) are important clinical drugs with anxiolytic, anticonvulsant, and sedative effects mediated by potentiation of inhibitory GABA type A receptors (GABA_ARs). Tolerance limits the clinical utility of BZDs, yet the mechanisms underlying tolerance after chronic exposure have not been thoroughly investigated. Here, we assessed the impact of chronic (7-day) treatment with the BZD diazepam (DZP) on the dynamic plasticity and subsynaptic organization of the gephyrin scaffold and γ2 subunit-containing GABA_ARs in primary neurons. After functional confirmation of diminished BZD sensitivity, we provide the first super-resolution analysis of inhibitory nanoscale plasticity induced by chronic BZD exposure: gephyrin subsynaptic domains were smaller and the inhibitory postsynaptic area was overall diminished by DZP treatment, resulting in a condensation of synaptic γ2-GABA_ARs into smaller synaptic areas. Using a novel fluorescence-based <i>in situ</i> proximity ligation assay and biochemical fractionation analysis, the mechanism for gephyrin downregulation was revealed to be dependent on phosphorylation and protease cleavage. Accordingly, DZP treatment impaired gephyrin synaptic stability, demonstrated by live-imaging photobleaching experiments. Despite the loss of BZD sensitivity and stable synaptic gephyrin, 7-day DZP treatment did not reduce the surface or total protein levels of BZD-sensitive γ2-GABA_ARs, as shown in prior short-term BZD treatment studies. Instead, chronic DZP treatment induced an accumulation of γ2-GABA_ARs in the extrasynaptic membrane. Surprisingly, γ2-GABA_AR interactions with gephyrin were also enriched extrasynaptically. An identified rise in extrasynaptically-localized gephyrin cleavage fragments may function to confine receptors away from the synapse, as supported by a decrease in extrasynaptic γ2-GABA_AR mobility. Altogether, we find that chronic BZD treatment triggers several subtle converging plasticity events at inhibitory synapses which effectively restrict the synaptic renewal of BZD-sensitive GABA_ARs via mechanisms distinct from those observed with short-term treatment.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1624813"},"PeriodicalIF":4.2,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144674239","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":"Tear deficiency transforms spatial distribution of corneal calcitonin gene-related peptide-positive nerves in rats.","authors":"Takeshi Kiyoi, Akihiro Nakajima, Qiang He, Li Liu, Shijie Zheng, Shizuka Kobayashi, Junsuke Uwada, Takayoshi Masuoka","doi":"10.3389/fncel.2025.1619310","DOIUrl":"10.3389/fncel.2025.1619310","url":null,"abstract":"<p><p>The nerve terminals distributed in the cornea are important for sensory perception and the maintenance of ocular surface homeostasis. In dry eye disease (DED), corneal nerves undergo functional and morphological changes that may be involved in abnormal ocular surface sensation and corneal pathology. However, changes in the spatial distribution of corneal nerves, including polymodal nociceptors, and their regulatory mechanisms remain unknown. In the present study, we analyzed time-dependent changes in corneal nerves, focusing on calcitonin gene-related peptide (CGRP)-positive nociceptive nerves in DED model rats, in which both the extraorbital and intraorbital lacrimal glands were surgically excised. After gland excision, the cornea showed acute inflammation, characterized by the presence of segmented-nucleus neutrophil infiltration, followed by chronic inflammation and angiogenesis. In parallel, denervation and subsequent reinnervation in the epithelium, as well as excessive innervation in the stroma, were observed, both involving CGRP-positive nerves. The DED rats showed hypoesthesia and subsequently hyperesthesia in response to mechanical stimulation of the corneal surface, which was synchronized with the denervation and reinnervation of corneal nerve plexuses in the epithelium. Persistent hyperalgesia to capsaicin in DED rats was not correlated with CGRP-positive nerve distribution in the early phase. After gland excision, the expression of neurotropic factor Sema7A increased within the epithelium and stroma, while that of the repulsive axon guidance factor Sema3A decreased in the epithelium. The expression patterns of these molecules correlate with reinnervation of the epithelium and excessive innervation of the stroma. These data suggest that changes in nerve distribution, including CGRP-positive nerves, might partially contribute to sensory perception and progression of corneal inflammatory pathology in DED. Sema3A and Sema7A may be involved in reinnervation as part of the regulatory mechanism in DED.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1619310"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642209","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":"Potassium channel clustering: mechanisms shaping axonal excitability.","authors":"Gabriel Escobedo, Matthew N Rasband","doi":"10.3389/fncel.2025.1627517","DOIUrl":"10.3389/fncel.2025.1627517","url":null,"abstract":"<p><p>The precise clustering of ion channels at axon initial segments (AIS) and nodes of Ranvier is essential for axonal excitability and rapid action potential propagation. Among the axonal ion channels, voltage-gated potassium channels (Kv) and two-pore domain potassium (K2P) leak channels are key regulators of AIS and nodal excitability. Kv7 and Kv1 channels contribute to action potential threshold and repolarization at the AIS, and membrane repolarization in axons has historically been attributed to Kv channels. However, recent studies suggest that at nodes of Ranvier K2P channels, particularly TRAAK and TREK-1, play a dominant role in action potential repolarization. The interaction of Kv and K2P channels with diverse scaffolding proteins ensures their precise localization at AIS and nodes. Mislocalization or dysfunction of axonal Kv and K2P channels can cause epilepsy and neurodevelopmental disorders. This review explores the diversity of potassium channels and the mechanisms responsible for their clustering at AIS and nodes of Ranvier. Understanding these processes will be essential for therapeutic strategies aimed at treating diseases characterized by abnormal potassium channel expression, clustering, and function in neurons.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1627517"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642208","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":"Sialylation as a checkpoint for inflammatory and complement-related retinal diseases.","authors":"Yiduo Min, German Cuevas-Rios, Thomas Langmann, Harald Neumann","doi":"10.3389/fncel.2025.1623755","DOIUrl":"10.3389/fncel.2025.1623755","url":null,"abstract":"<p><p>Sialylation is a modification process involving the addition of sialic acid residues to the termini of glycoproteins and glycolipids in mammalian cells. Sialylation serves as a crucial checkpoint inhibitor of the complement and immune systems, particularly within the central nervous system (CNS), including the retina. Complement factor H (FH), complement factor properdin (FP), and sialic acid-binding immunoglobulin-like lectin (SIGLEC) receptors of retinal mononuclear phagocytes are key players in regulating the complement and innate immune systems in the retina by recognizing sialic acid (Sia) residues. Intact retinal sialylation prevents any long-lasting and excessive complement or immune activation in the retina. However, sialylated glycolipids are reduced in the CNS with aging, potentially contributing to chronic inflammatory processes in the retina. Particularly, genetically induced hyposialylation in mice leads to age-related, complement factor C3-mediated retinal inflammation and bipolar cell loss. Notably, most of the gene transcript pathways enriched in the mouse retina, following genetically induced hyposialylation, are also involved in age-related macular degeneration (AMD). Interestingly, intravitreal application of polysialic acid (polySia) controlled the innate immune responses in the mouse retina by blocking mononuclear phagocyte reactivity, inhibiting complement activation, and protecting against vascular damage in two different humanized SIGLEC-11 animal models. Accordingly, a polySia polymer conjugate has entered clinical phase II/III testing in patients with geographic atrophy secondary to AMD. Thus, hyposialylation or dysfunctional sialylation should be considered as an age-related contributor to inflammatory retinal diseases, such as AMD. Consequently, sialic acid-based biologics could provide novel therapies for complement-related retinal diseases.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1623755"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625750","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":"PTEN in somatostatin neurons regulates fear and anxiety and is required for inhibitory synaptic connectivity within central amygdala.","authors":"Timothy W Holford, Kaitlyn N Letourneau, Carolyn Von-Walter, Daniela Moncaleano, Cody L Loomis, M McLean Bolton","doi":"10.3389/fncel.2025.1597131","DOIUrl":"10.3389/fncel.2025.1597131","url":null,"abstract":"<p><strong>Introduction: </strong>The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a negative regulator of the mTOR pathway and is strongly associated with autism spectrum disorder (ASD), with up to 25% of ASD patients with macrocephaly harboring PTEN mutations. Mice with germline PTEN haploinsufficiency show behavioral characteristics resembling ASD, as do various mouse models with conditional knockouts of PTEN. Human tissue studies and those from multiple genetic mouse models suggest that dysfunction of GABAergic interneurons may play a role in the development of ASD, but the precise mechanisms remain elusive. PTEN provides a target for investigation because it regulates the development of inhibitory neurons arising from the medial ganglionic eminence, promoting the survival and maturation of parvalbumin (PV+) neurons at the expense of somatostatin (SOM+) neurons.</p><p><strong>Methods: </strong>Here, we investigate how PTEN regulates SOM+ neurons at the cellular and circuit level in the central lateral amygdala (CeL), an area that governs the key ASD behavioral symptoms of social anxiety and altered emotional motivation for social engagement using behavioral analysis, electrophysiology, and two-photon local circuit mapping.</p><p><strong>Results: </strong>We found that knocking out PTEN in SOM+ neurons results in elevated levels of fear and anxiety and decreases CeL local circuit connectivity. Specifically, this manipulation decreased the strength of connections between individual neurons and altered the distribution of local connections in a cell-type specific manner. In contrast to the deficit in local inhibitory connections within CeL, the excitatory drive from the major CeL input, the basolateral amygdala (BLA) was enhanced.</p><p><strong>Discussion: </strong>This combined imbalance of enhanced excitation and diminished local inhibition likely underlies the heightened fear learning and anxiety we observed in the PTEN-SOM-KO mice.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1597131"},"PeriodicalIF":4.2,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607921","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 role of oxidative stress in spinal cord ischemia reperfusion injury: mechanisms and therapeutic implications.","authors":"Yu Xing, Yuan-Zhang Xiao, Min Zhao, Jiang-Jun Zhou, Kai Zhao, Chun-Lin Xiao","doi":"10.3389/fncel.2025.1590493","DOIUrl":"10.3389/fncel.2025.1590493","url":null,"abstract":"<p><p>Spinal cord ischemia/reperfusion injury (SCIRI) is a serious disease that leads to the loss of sensory and motor functions and is a common complication after spinal cord injury, spinal cord degeneration or thoracic and abdominal aortic surgery. At present, the spinal cord is mainly protected from ischemic injury through treatment strategies such as hypothermia, surgery and drug assistance, but these intervention measures cannot effectively improve these conditions. SCIRI is a complex process that leads to cell damage and death. Among them, oxidative stress is an important pathological event of ischemia/reperfusion injury. Oxidative stress can initiate multiple inflammatory and apoptotic pathways, triggering a series of destructive events such as inflammatory responses and cell death, further deteriorating the microenvironment at the injured site, and leading to neurological dysfunction. Based on the important role of oxidative stress in SCIRI, we believe that targeted inhibition of oxidative stress responses can effectively reduce secondary injuries caused by trauma, which has a certain positive effect on the rehabilitation and prognosis of patients with SCIRI. This review systematically expounds the spatiotemporal dynamic characteristics of oxidative stress during the SCIRI process and its molecular regulatory network, with a focus on analyzing the multivariate generation mechanism of ROS. To deeply explore the regulatory effects of ROS on pathological processes such as neuronal death, inflammatory response and blood-spinal barrier disruption under SCIRI conditions, as well as its interaction patterns with signaling pathways. In order to form a systematic treatment for SCIRI caused by oxidative stress and promote the recovery of neurological function after injury. This review is helpful for us to understand the effect of oxidative stress on SCIRI and provides a theoretical basis for the treatment of SCIRI based on oxidative stress.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1590493"},"PeriodicalIF":4.2,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590843","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":"Corrigendum: <i>O</i> ⁶-methylguanine DNA methyltransferase (MGMT) expression in U1242 glioblastoma cells enhances <i>in vitro</i> clonogenicity, tumor implantation <i>in vivo</i>, and <i>sensitivity</i> to alisertib-carboplatin combination treatment.","authors":"Müge Sak, Brian J Williams, Andrew J Hey, Mayur Sharma, Leslie Schier, Megan J Wilson, Mahatma Ortega, Alyssa I Lara, Mikaela N Brentlinger, Norman L Lehman","doi":"10.3389/fncel.2025.1637837","DOIUrl":"10.3389/fncel.2025.1637837","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2025.1552015.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1637837"},"PeriodicalIF":4.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590842","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":"Knockdown and overexpression of basolateral amygdala SIRT1 via AAV bidirectionally alter morphine-induced conditioned place preference extinction in mice.","authors":"Guo Hao, Yao Mingchen, Zheng Yalin, Qu Yaqi, Yang Tingwu, Xing Xinru, Li Kaixuan, Dong Yani, Liu Dongsen","doi":"10.3389/fncel.2025.1604914","DOIUrl":"10.3389/fncel.2025.1604914","url":null,"abstract":"<p><strong>Introduction: </strong>This study investigates the role of SIRT1 in basolateral amygdala (BLA) glutamatergic neurons in morphine-induced conditioned place preference (CPP).</p><p><strong>Methods: </strong>Via SIRT1 knockdown/overexpression in bilateral BLA of morphine-induced CPP mice. Outcomes measured by behavioral tests, WB, and transmission electron microscopy.</p><p><strong>Results: </strong>We found that SIRT1 knockdown prolonged CPP extinction and enhanced reinstatement, whereas overexpression accelerated extinction and attenuated relapse. Behavioral tests revealed that SIRT1 knockdown rescued morphine-induced memory impairment and anxiety-like behaviors, while overexpression exacerbated these effects. Ultrastructural and molecular analyses demonstrated SIRT1 modulation of synaptic plasticity-related proteins (BDNF, PSD95) and synaptic ultrastructure in BLA.</p><p><strong>Discussion: </strong>Our findings reveal that SIRT1 bidirectionally regulates opioid-associated memory persistence through synaptic remodeling, highlighting its potential as an epigenetic target for addiction treatment. While SIRT1 is implicated in neuroplasticity, its specific role in modulating opioid-associated memory circuits within the BLA remains undefined, representing a critical gap in understanding addiction neuropathology.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1604914"},"PeriodicalIF":4.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575206","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":"Evaluation of retinal structure changes with AI-based OCT image segmentation for sodium iodate induced retinal degeneration.","authors":"Yong Zeng, Jiaming Zhou, Yichao Li, Bruno Alvisio, Jacob Czech, David Bissig, Haohua Qian","doi":"10.3389/fncel.2025.1605639","DOIUrl":"10.3389/fncel.2025.1605639","url":null,"abstract":"<p><p>Segmentations of retinal optical coherence tomography (OCT) images provide valuable information about each specific retinal layer. However, processing images from degenerative retina remains challenging. This study developed artificial intelligence (AI)-based segmentation to analyze structure changes in sodium iodate (SI)-treated mice. The software is capable of segmenting seven retinal layers and one choroid layer. Analyzing OCT images captured at days post SI-injection (PI) revealed early changes in the retinal pigment epithelium (RPE) layer, with increase in thickness and reduction in reflectance calculated by estimated Attenuation Coefficients (eAC). On the other hand, eAC for outer nuclear layer (ONL) exhibited early and sustained increase after SI treatment. SI induced exponential reduction in ONL thickness with a half-reduction time of about 3 days, indicating progressive photoreceptor degeneration. The extent of degeneration was correlated with ONL eAC level at PI1. Inner retinal layers showed bi-phasic reactions, with initial increases in layer thickness that peaked at around PI3, followed by gradual reduction to lower than baseline levels. In addition, SI also induced transient increases in vitreous particles concentrated around the optic nerve head. Furthermore, there was a gradual reduction of choroid thickness after SI treatment. These results indicate the AI-segmentation tool's usefulness for providing a sensitive and accurate assessment of structure changes in diseased retina and revealed more detailed characterization of SI-induced degeneration in all retinal layers with distinct time courses. Our results also support ONL reflectance changes as an early biomarker for retinal degeneration.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1605639"},"PeriodicalIF":4.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12213626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552825","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}