Frontiers in Cellular Neuroscience最新文献

{"title":"Traversing the epigenetic landscape: DNA methylation from retina to brain in development and disease.","authors":"Chunxiu Xu, Xuefei Fu, Huan Qin, Kai Yao","doi":"10.3389/fncel.2024.1499719","DOIUrl":"10.3389/fncel.2024.1499719","url":null,"abstract":"<p><p>DNA methylation plays a crucial role in development, aging, degeneration of various tissues and dedifferentiated cells. This review explores the multifaceted impact of DNA methylation on the retina and brain during development and pathological processes. First, we investigate the role of DNA methylation in retinal development, and then focus on retinal diseases, detailing the changes in DNA methylation patterns in diseases such as diabetic retinopathy (DR), age-related macular degeneration (AMD), and glaucoma. Since the retina is considered an extension of the brain, its unique structure allows it to exhibit similar immune response mechanisms to the brain. We further extend our exploration from the retina to the brain, examining the role of DNA methylation in brain development and its associated diseases, such as Alzheimer's disease (AD) and Huntington's disease (HD) to better understand the mechanistic links between retinal and brain diseases, and explore the possibility of communication between the visual system and the central nervous system (CNS) from an epigenetic perspective. Additionally, we discuss neurodevelopmental brain diseases, including schizophrenia (SZ), autism spectrum disorder (ASD), and intellectual disability (ID), focus on how DNA methylation affects neuronal development, synaptic plasticity, and cognitive function, providing insights into the molecular mechanisms underlying neurodevelopmental disorders.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1499719"},"PeriodicalIF":4.2,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827867","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 underlying molecular mechanisms of Fyn in neonatal hypoxic-ischaemic encephalopathy.","authors":"Jiao Zhou, Xiang Lu, Haichuan Wang","doi":"10.3389/fncel.2024.1476856","DOIUrl":"10.3389/fncel.2024.1476856","url":null,"abstract":"<p><p>Fyn is a cytoplasmic tyrosine kinase (TK) that is a nonreceptor and a member of the Src family of kinases (SFKs). It is involved in several transduction pathways in the central nervous system (CNS), such as oligodendrocyte development, myelination, axon guidance, and synaptic transmission. Owing to its wide range of activities in the molecular signaling pathways that underpin both neuropathologic and neurodevelopmental events, Fyn has remained of great interest for more than a century. Accumulating preclinical data have highlighted the potential role of Fyn in the pathophysiology of neonatal hypoxic-ischaemic encephalopathy (HIE). By mediating important signaling pathways, Fyn may control glutamate excitotoxicity, promote neuroinflammation and facilitate the death of neurons caused by oxidative stress. In this review, we address new evidence regarding the role of Fyn in the pathogenesis of this condition, with the aim of providing a reference for the development of new strategies to improve the prognosis of neonatal HIE. In addition, we also offer insights into additional Fyn-related molecular mechanisms involved in HIE pathology.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1476856"},"PeriodicalIF":4.2,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11631624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812468","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 BE (2)-M17 neuroblastoma cell line: revealing its potential as a cellular model for Parkinson's disease.","authors":"Angel Carvajal-Oliveros, Camila Román-Martínez, Enrique Reynaud, Eduardo Martínez-Martínez","doi":"10.3389/fncel.2024.1485414","DOIUrl":"10.3389/fncel.2024.1485414","url":null,"abstract":"<p><p>Parkinson's disease is a pathology with a wide range of <i>in vivo</i> and <i>in vitro</i> models available. Among these, the SH-SY5Y neuroblastoma cell line is one of the most employed. This model expresses catecholaminergic markers and can differentiate and acquire various neuronal phenotypes. However, challenges persist, primarily concerning the variability of growth media, expression of dopaminergic markers, and a wide variety of differentiation protocols have been reported in the literature without direct comparison between them. This lack of standardized differentiation conditions impacts result reproducibility and it makes it very difficult to compare the results obtained from different research groups. An alternative cellular model is the neuroblastoma BE (2)-M17 which exhibits a high basal expression of numerous dopaminergic markers such as tyrosine hydroxylase (TH), vesicular monoamine transporter 2 (VMAT2), and dopamine transporter (DAT). The BE (2)-M17 cells show neuronal properties, grows rapidly in conventional media, and can easily be differentiated to increase their dopaminergic phenotype. In this review, we will thoroughly explore the properties of the BE (2)-M17 cell line and discuss its potential as an excellent model for studying Parkinson's disease.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1485414"},"PeriodicalIF":4.2,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806683","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":"Interlaminar and varicose-projection astrocytes: toward a new understanding of the primate brain.","authors":"Caterina Ciani, Carmen Falcone","doi":"10.3389/fncel.2024.1477753","DOIUrl":"10.3389/fncel.2024.1477753","url":null,"abstract":"<p><p>In the last years, science started to move toward a more <i>glio-neurocentric</i> view, in which astrocytes are hypothesized to be directly involved in cognitive functions. Indeed, astrocytes show a variety of shapes with species-specific characteristics, suggesting a specialization of roles during evolution. Interlaminar (ILA) and varicose-projection (VP-As) astrocytes show an anatomical organization that is different compared to the classical horizontal net typically formed by protoplasmic and fibrous astrocytes. ILAs show a modular architecture with the soma in the first cortical layer and processes toward the deep layers with species-specific length. VP-As reside in the deep layers of the cortex, are characterized by varicosities on the longest processes, and are individual-specific. These characteristics suggest roles that are more complex than what was theorized until now. Here, we recapitulate what we know so far from literature from the first time ILAs were described to the most recent discoveries, spanning from morphology description, hypothesis on the development to their features in diseases. For a complete glance on this topic, we included a final paragraph on which techniques and models were used to study ILAs and VP-As, and what new avenues may be opened thanks to more novel methods.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1477753"},"PeriodicalIF":4.2,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800091","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":"Regulation of cochlear hair cell function by intracellular calcium stores.","authors":"Ghanshyam P Sinha, Gregory I Frolenkov","doi":"10.3389/fncel.2024.1484998","DOIUrl":"10.3389/fncel.2024.1484998","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Mammalian hearing depends on the dual mechanosensory and motor functions of cochlear hair cells. Both these functions may be regulated by Ca&lt;sup&gt;2+&lt;/sup&gt; release from intracellular stores. However, it is still unclear how exactly intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; release may affect either hair cell mechano-electrical transduction (MET) or prestin-dependent electromotility in outer hair cells (OHCs).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Here, we used photo-activatable (caged) compounds to generate fast increases of either Ca&lt;sup&gt;2+&lt;/sup&gt; or inositol-3-phosphate (IP&lt;sub&gt;3&lt;/sub&gt;) in the cytosol of young postnatal rodent auditory hair cells, thereby stimulating either Ca&lt;sup&gt;2+&lt;/sup&gt;- or IP&lt;sub&gt;3&lt;/sub&gt;- induced releases of Ca&lt;sup&gt;2+&lt;/sup&gt; from intracellular stores. Fast Ca&lt;sup&gt;2+&lt;/sup&gt; imaging was used to monitor propagation of Ca&lt;sup&gt;2+&lt;/sup&gt; signals along the length of a hair cell. To access potential physiological role(s) of intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; releases, we used whole cell patch clamp to record: i) OHC voltage-dependent capacitance, a known electrical correlate of prestin-based electromotility, and ii) MET currents evoked by stereocilia bundle deflections with fluid-jet. In the latter experiments, changes of mechanical stiffness of the hair bundles were also quantified from video recordings of stereocilia movements.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Ca&lt;sup&gt;2+&lt;/sup&gt; uncaging at the OHC apex initiated Ca&lt;sup&gt;2+&lt;/sup&gt; wave propagating to the base of the cell with subsequent Ca&lt;sup&gt;2+&lt;/sup&gt; build-up there. Ca&lt;sup&gt;2+&lt;/sup&gt; uncaging at the OHC base generated long-lasting and apparently self-sustained Ca&lt;sup&gt;2+&lt;/sup&gt; responses, further confirming Ca&lt;sup&gt;2+&lt;/sup&gt;-induced Ca&lt;sup&gt;2+&lt;/sup&gt; release in the OHC basal region. Photoactivated IP&lt;sub&gt;3&lt;/sub&gt; initiated a slow increase of cytosolic Ca&lt;sup&gt;2+&lt;/sup&gt; ([Ca&lt;sup&gt;2+&lt;/sup&gt;] &lt;sub&gt;&lt;i&gt;i&lt;/i&gt;&lt;/sub&gt; ) throughout the whole OHC, confirming the presence of slow-activated IP&lt;sub&gt;3&lt;/sub&gt;-gated Ca&lt;sup&gt;2+&lt;/sup&gt; stores in OHCs. Interestingly, Ca&lt;sup&gt;2+&lt;/sup&gt; uncaging produced no effects on OHC voltage-dependent capacitance. In an OHC, the rise of [Ca&lt;sup&gt;2+&lt;/sup&gt;] &lt;sub&gt;&lt;i&gt;i&lt;/i&gt;&lt;/sub&gt; is known to decrease axial stiffness of the cell and may modulate the stiffness of mechanosensory stereocilia bundles. To separate these two phenomena, we explored the potential effects of intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; release on mechanical properties of stereocilia bundles in cochlear inner hair cells (IHCs). Ca&lt;sup&gt;2+&lt;/sup&gt; uncaging at the apex of an IHC caused a long-lasting increase in mechanical stiffness of stereocilia bundle without any changes in the amplitude or deflection sensitivity of the MET current.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;We concluded that the most likely physiological role of IP&lt;sub&gt;3&lt;/sub&gt;-gated Ca&lt;sup&gt;2+&lt;/sup&gt; release at the apex of the cell is the regulation of hair bundle stiffness. In contrast, Ca&lt;sup&gt;2+&lt;/sup&gt;-induced Ca&lt;sup&gt;2+&lt;/sup&gt; release at the base of OHCs seems to regulate","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1484998"},"PeriodicalIF":4.2,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11625566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800023","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":"Retraction: Effect of histone deacetylase inhibitors trichostatin A and valproic acid on hair cell regeneration in zebrafish lateral line neuromasts.","authors":"","doi":"10.3389/fncel.2024.1530876","DOIUrl":"https://doi.org/10.3389/fncel.2024.1530876","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3389/fncel.2014.00382.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1530876"},"PeriodicalIF":4.2,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800024","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":"LAMTOR1 regulates dendritic lysosomal positioning in hippocampal neurons through TRPML1 inhibition.","authors":"Jiandong Sun, Weiju Lin, Xiaoning Hao, Michel Baudry, Xiaoning Bi","doi":"10.3389/fncel.2024.1495546","DOIUrl":"10.3389/fncel.2024.1495546","url":null,"abstract":"<p><p>Intracellular lysosomal trafficking and positioning are fundamental cellular processes critical for proper neuronal function. Among the diverse array of proteins involved in regulating lysosomal positioning, the Transient Receptor Potential Mucolipin 1 (TRPML1) and the Ragulator complex have emerged as central players. TRPML1, a lysosomal cation channel, has been implicated in lysosomal biogenesis, endosomal/lysosomal trafficking including in neuronal dendrites, and autophagy. LAMTOR1, a subunit of the Ragulator complex, also participates in the regulation of lysosomal trafficking. Here we report that LAMTOR1 regulates lysosomal positioning in dendrites of hippocampal neurons by interacting with TRPML1. LAMTOR1 knockdown (KD) increased lysosomal accumulation in proximal dendrites of cultured hippocampal neurons, an effect reversed by TRPML1 KD or inhibition. On the other hand, TRPML1 activation with ML-SA1 or prevention of TRPML1 interaction with LAMTOR1 using a TAT-decoy peptide induced dendritic lysosomal accumulation. LAMTOR1 KD-induced proximal dendritic lysosomal accumulation was blocked by the dynein inhibitor, ciliobrevin D, suggesting the involvement of a dynein-mediated transport. These results indicate that LAMTOR1-mediated inhibition of TRPML1 is critical for normal dendritic lysosomal distribution and that release of this inhibition or direct activation of TRPML1 results in abnormal dendritic lysosomal accumulation. The roles of LAMTOR1-TRPML1 interactions in lysosomal trafficking and positioning could have broad implications for understanding cognitive disorders associated with lysosomal pathology and calcium dysregulation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1495546"},"PeriodicalIF":4.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11621854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800094","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":"Neuroinflammation and major depressive disorder: astrocytes at the crossroads.","authors":"Melissa Puentes-Orozco, Sonia L Albarracin, María Marcela Velásquez","doi":"10.3389/fncel.2024.1504555","DOIUrl":"10.3389/fncel.2024.1504555","url":null,"abstract":"<p><p>Major depressive disorder is a complex and multifactorial condition, increasingly linked to neuroinflammation and astrocytic dysfunction. Astrocytes, along with other glial cells, beyond their classic functions in maintaining brain homeostasis, play a crucial role in regulating neuroinflammation and neuroplasticity, key processes in the pathophysiology of depression. This mini-review explores the involvement of astrocytes in depression emphasizing their mediation in neuroinflammation processes, the impact of astrocytic dysfunction on neuroplasticity, and the effect of some antidepressants on astrocyte reactivity. Recent evidence suggests that targeting astrocyte-related signaling pathways, particularly the balance between different astrocytic phenotypes, could offer promising evidence for therapeutic strategies for affective disorders. Therefore, a deeper understanding of astrocyte biology may open the way to innovative treatments aimed at mitigating depressive symptoms by impacting both neuroinflammation and imbalances in neuroplasticity.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1504555"},"PeriodicalIF":4.2,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11620873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800020","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":"A crosstalk between autophagy and apoptosis in intracerebral hemorrhage.","authors":"Moyan Wang, Xin Chen, Shuangyang Li, Lingxue Wang, Hongmei Tang, Yuting Pu, Dechou Zhang, Bangjiang Fang, Xue Bai","doi":"10.3389/fncel.2024.1445919","DOIUrl":"10.3389/fncel.2024.1445919","url":null,"abstract":"<p><p>Intracerebral hemorrhage (ICH) is a severe condition that devastatingly harms human health and poses a financial burden on families and society. Bcl-2 Associated X-protein (Bax) and B-cell lymphoma 2 (Bcl-2) are two classic apoptotic markers post-ICH. Beclin 1 offers a competitive architecture with that of Bax, both playing a vital role in autophagy. However, the interaction between Beclin 1 and Bcl-2/Bax has not been conjunctively analyzed. This review aims to examine the crosstalk between autophagy and apoptosis in ICH by focusing on the interaction and balance of Beclin 1, Bax, and Bcl-2. We also explored the therapeutic potential of Western conventional medicine and traditional Chinese medicine (TCM) in ICH via controlling the crosstalk between autophagy and apoptosis.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1445919"},"PeriodicalIF":4.2,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142800088","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":"Bridging the gap of vision restoration.","authors":"Maya Carleton, Nicholas W Oesch","doi":"10.3389/fncel.2024.1502473","DOIUrl":"10.3389/fncel.2024.1502473","url":null,"abstract":"<p><p>Retinitis pigmentosa (RP) and Age-Related Macular Degeneration (AMD) are similar in that both result in photoreceptor degeneration leading to permanent progressive vision loss. This affords the possibility of implementing vision restoration techniques, where light signaling is restored to spared retinal circuitry to recreate vision. There are far more AMD patients (Wong et al., 2014), yet more resources have been put towards researching and developing vision restoration strategies for RP despite it rarity, because of the tractability of RP disease models. The hope is that these therapies will extend to the AMD population, however, many questions remain about how the implementation of prosthetic or optogenetic vision restoration technologies will translate between RP and AMD patients. In this review, we discuss the difference and similarities of RP and AMD with a focus on aspects expected to impact vision restoration strategies, and we identify key gaps in knowledge needed to further improve vision restoration technologies for a broad patient population.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1502473"},"PeriodicalIF":4.2,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11617155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784409","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}