Developmental Neurobiology最新文献

{"title":"Investigating the Effect of Capric Acid on Antibiotic-Induced Autism-Like Behavior in Rodents.","authors":"Nikhila Shekhar, Ajit Kumar Thakur","doi":"10.1002/dneu.22959","DOIUrl":"https://doi.org/10.1002/dneu.22959","url":null,"abstract":"<p><p>Owing to the high prevalence of gastrointestinal dysfunction in patients, the gut-brain axis is considered to play a vital role in neurodevelopment diseases. Recent pieces of evidence have pointed to the usage of antibiotics at an early developmental stage to be a causative factor in autism due to its ability to induce critical changes in the gut microbiota. The purpose of the study is to determine the neuroprotective effect of capric acid (CA) on autism in antibiotic-induced gut dysbiosis in rodents. In this study, the effect of CA was observed in penicillin V (31 mg/kg, p.o.) exposed animals by evaluating their autism-like behavioral and biochemical parameters. The establishment of gut dysbiosis was confirmed by 16 RNA sequencing, and behavioral tests were performed. Subsequently, oxidative stress, cytokine levels, and mitochondrial complex activities in the hippocampus and prefrontal cortex were analyzed. It was observed that the administration of penicillin V during the perinatal period produced gut dysbiosis and long-lasting changes in social behavior with symptoms of anxiety and depression and impaired learning and memory. Treatment with penicillin V also produced oxidative stress, mitochondrial dysfunction, and inflammation in the hippocampus and prefrontal cortex. Treatment with CA produced a positive effect on the alterations with maximum effects evident at 400 mg/kg, p.o. through amelioration of behavioral as well as biochemical changes. The current study concluded that CA could act as a likely candidate for the treatment and management of autism via modulation of gut dysbiosis-induced neurobehavioral parameters, oxidative stress, mitochondrial dysfunction, and inflammatory markers.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 1","pages":"e22959"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Neurodiversity Framework in Medicine: On the Spectrum.","authors":"Raul Miranda-Ojeda, Anuksha Wickramasinghe, Georgios Ntolkeras, Isabel Castanho, Walid Yassin","doi":"10.1002/dneu.22960","DOIUrl":"https://doi.org/10.1002/dneu.22960","url":null,"abstract":"<p><p>The term \"neurodiversity\" refers to the natural heterogeneity in human neurological functioning, which includes neurodevelopmental differences and other mental health conditions (e.g., autism spectrum disorder [ASD], attention-deficit hyperactivity disorder [ADHD], dyslexia, bipolar disorder, schizophrenia, and depression). This new viewpoint has significant consequences for the future of medicine, specifically in psychiatry, neurology, and neurodevelopmental medicine, as it undermines established notions of these conditions as disorders/diseases that may be healed or corrected. The neurodiversity approach, on the other hand, acknowledges these divergences as natural variations, calling for tailored support and interventions that accommodate individual needs. Neurodiversity could impact current medical perspectives by supporting a shift from pathology to identity. Rather than focusing on the difficulties associated with a specific ailment, the neurodiversity approach stresses the strengths and distinct perspectives that come with neurodivergent identities. This shift has significant consequences for research and therapy by fostering the development of innovative treatments aimed at increasing quality of life and improving functional results. This new perspective advocates including neurodivergent people in all sectors of society, including research, clinical practice, and policymaking, by recognizing, accepting, and integrating natural variances in brain functioning. In this article, we review the development of the neurodiversity movement and propose \"The Neurodiversity Framework in Medicine,\" which challenges traditional views by recognizing neurological differences as natural variations, advocating for inclusive, person-centered approaches in healthcare.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 1","pages":"e22960"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated Serum Homocysteine Levels Impair Embryonic Neurodevelopment by Dysregulating the Heat Shock Proteins.","authors":"Jia Mai, Ling Yang, Min Wang, Jia-Min Deng, Min Min, Hong-Jian Xie, Yong-Mei Jiang, Hua-Qin Sun, Xiao-Juan Liu","doi":"10.1002/dneu.22958","DOIUrl":"https://doi.org/10.1002/dneu.22958","url":null,"abstract":"<p><p>Observational studies have found that elevated serum homocysteine (Hcy) levels during pregnancy may be associated with the occurrence of neural tube defects (NTDs). However, the effect of Hcy on fetal neural development and its underlying molecular mechanisms remains unclear. To uncover the molecular mechanism, we analyzed the serum Hcy concentration in pregnant women with normal and abnormal pregnancy outcomes and treated zebrafish model embryos with high Hcy. Our findings indicate that elevated serum Hcy levels during pregnancy are associated with adverse pregnancy outcomes. Using the zebrafish model and transcriptome analysis, we found that high Hcy levels led to developmental neural malformations in embryos and affected the expression of key genes at various stages of neural development. Interestingly, deep transcriptome analysis showed that dysregulated heat shock proteins (HSP) might play a key role in high Hcy-mediated alterations in neural development. Importantly, the inhibition of HSP significantly restored the embryonic neuroteratogenic effects induced by high Hcy levels in the zebrafish model. In summary, our findings provide a novel molecular pathogenic mechanism in which ectopic HSP is associated with neural development defects caused by high Hcy levels, suggesting potential prevention and targeted therapies for high Hcy level-related NTDs during pregnancy.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 1","pages":"e22958"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Transgenic Zebrafish Lines to Study the CHRNA3-B4-A5 Gene Cluster","authors":"Yuanqi Hua,&nbsp;Judith Habicher,&nbsp;Matthias Carl,&nbsp;Remy Manuel,&nbsp;Henrik Boije","doi":"10.1002/dneu.22956","DOIUrl":"10.1002/dneu.22956","url":null,"abstract":"<p>Acetylcholine (ACh), a vital neurotransmitter for both the peripheral (PNS) and central nervous systems (CNS), signals through nicotinic ACh receptors (nAChRs) and muscarinic ACh receptors (mAChR). Here, we explore the expression patterns of three nAChR subunits, <i>chrna3</i>, <i>chrnb4</i>, and <i>chrna5</i>, which are located in an evolutionary conserved cluster. This close genomic positioning, in a range of vertebrates, may indicate co-functionality and/or co-expression. Through novel transgenic zebrafish lines, we observe widespread expression within both the PNS and CNS. In the PNS, we observed expression of <i>chrna3^tdTomato</i>, <i>chrnb4^eGFP</i>, and <i>chrna5</i>^tdTomato in the intestinal enteric nervous system; <i>chrna5^tdTomato</i> and <i>chrnb4^eGFP</i> in sensory ganglia of the lateral line; and <i>chrnb4^eGFP</i> in the ear. In the CNS, the expression of <i>chrnb4^eGFP</i> and <i>chrna5</i>^tdTomato was found in the retina, all three expressed in diverse regions of the brain, where a portion of <i>chrna3^tdTomato</i> and <i>chrnb4^eGFP</i> cells were found to be inhibitory efferent neurons projecting to the lateral line. Within the spinal cord, we identify distinct populations of <i>chrna3^tdTomato</i>-, <i>chrnb4^eGFP</i>-, and <i>chrna5</i>^tdTomato-expressing neurons within the locomotor network, including <i>dmrt3a</i>-expressing interneurons and <i>mnx1</i>-expressing motor neurons. Notably, three to four primary motor neurons per hemisegment were labeled by both <i>chrna3^tdTomato</i> and <i>chrnb4^eGFP</i>. Interestingly, we identified an sl-type secondary motor neuron per hemisegement that strongly expressed <i>chrna5</i>^tdTomato and co-expressed <i>chrnb4^eGFP</i>. These transgenic lines provide insights into the potential roles of nAChRs within the locomotor network and open avenues for exploring their role in nicotine exposure and addiction in a range of tissues throughout the nervous system.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dneu.22956","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142834493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Cannabidiol Isolated or in Association With Risperidone in an Animal Model of Autism","authors":"Maiara de Aguiar da Costa,&nbsp;Gustavo Zanette Fernandes,&nbsp;Eduarda Maiochi,&nbsp;Maria Fernanda Pedro Ebs,&nbsp;Flávia da Silva Darós,&nbsp;Sofia Januário Bolan,&nbsp;Rosiane Ronchi Nascimento Costa,&nbsp;Victória Linden de Rezende,&nbsp;Gláucia Crispim da Silva,&nbsp;Rafael Mariano Bitencourt,&nbsp;Cinara Ludvig Gonçalves","doi":"10.1002/dneu.22955","DOIUrl":"10.1002/dneu.22955","url":null,"abstract":"<div>\u0000 \u0000 <p>Autism spectrum disorder (ASD) is characterized by deficits in communication, social interaction, and repetitive and stereotyped behaviors, with no specific drug therapy available. Studies have found that cannabidiol (CBD) can improve hyperactive and cognitive symptoms in children with ASD. However, little is known about the effect of CBD in combination with other medications, such as risperidone (RISP). This study aimed to evaluate the behavioral and biochemical effects of CBD in animals using a valproic acid (VPA)-induced ASD animal model. VPA was administered in pregnant Wistar rats on Day 12.5 of gestation to induce the ASD model. From the 10th to the 16th postnatal day (PND), the neurodevelopment of the animals was assessed through eye-opening, olfactory discrimination, and negative geotaxis behavioral tests. From PNDs 9 to 54, the animals were weighed. They were treated for 21 days with CBD alone (100 mg/kg, by gavage, twice a day) or in combination with RISP (0.1 mg/kg, by gavage, once a day). At PND 55, the animals were evaluated in social interaction and locomotor activity experiments. Finally, after behavioral assessment, the animals were euthanized, the brain was isolated, and oxidative stress parameters were evaluated in the hippocampus and cortex posterior. Animals exposed to VPA showed neurodevelopmental delays in opening their eyes, difficulties in turning around their axis, and took longer time to find the original nest when compared to control animals. They also exhibited impaired sociability and reduced exploratory activity, which indicates model impairments. Interestingly, animals exposed to VPA treated with CBD + RISP significantly improved sociability parameters, whereas isolated CBD did not affect this parameter. In the biochemical analysis, a significant decrease in the hippocampal sulfhydryl content was noted in the CT + CBD group and an increase in the VPA + CBD group. In conclusion, these results suggest that CBD, in combination with RISP, may be an interesting pharmacological approach to reducing ASD-related symptoms.</p>\u0000 <p><b>Summary</b>: Besides the increased prevalence of ASD cases in recent years, there are no medications to improve the central symptoms of autism. Numerous studies discuss CBD as an important medication for improving ASD symptoms; however, it is not known how CBD interacts with commonly used drugs in ASD individuals, such as RISP. This study demonstrated that CBD therapy, only when combined with RISP, improved sociability in a VPA-induced ASD animal model.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defective Hippocampal Primary Ciliary Function and Aberrant LKB1/AMPK Signaling Pathway Are Associated With the Inhibition of Autophagic Activity in Offspring Born to Mothers of Advanced Maternal Age","authors":"Ziyao Han,&nbsp;Xiaoyue Yang,&nbsp;Jianxiong Gui,&nbsp;Hanyu Luo,&nbsp;Dishu Huang,&nbsp;Hengsheng Chen,&nbsp;Li Cheng,&nbsp;Ping Yuan,&nbsp;Li Jiang","doi":"10.1002/dneu.22954","DOIUrl":"10.1002/dneu.22954","url":null,"abstract":"<div>\u0000 \u0000 <p>Advanced maternal age (AMA) negatively influences the development and cognitive functions of offspring. However, the underlying mechanism remains to be elucidated. As hippocampal autophagy and primary cilia play a crucial role in learning and memory abilities, this study aimed to investigate the effects of AMA on hippocampal autophagy and primary cilia, and to explore their relationship with the changes of LKB1/AMPK signaling pathway in offspring rats. The whole brains and hippocampus of offspring born to 12-month-old (AMA) and 3-month-old (control) Sprague–Dawley (SD) female rats were collected on post-natal days (P) 14, 28, and 60. Transmission electron microscopy was employed to count the number of autophagosomes. The quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting were used to quantify gene expression, and immunofluorescence was used to measure primary cilia. The results revealed that autophagic activity was inhibited from childhood to adulthood in the AMA group. Furthermore, in the early developmental stage, primary ciliogenesis and growth in the hippocampus in the AMA group were impaired, with astrocytes being more severely affected. In addition, the AMA group exhibited an abnormal activation of the LKB1/AMPK signaling pathway. Thus, in offspring born to mothers of AMA, impaired hippocampal primary ciliary function and aberrant activation of the LKB1/AMPK signaling pathway are associated with inhibited autophagic activity.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"85 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellularity Defects Are Not Ubiquitous in the Brains of Fetuses With Down Syndrome","authors":"Marco Emili,&nbsp;Fiorenza Stagni,&nbsp;Maria Paola Bonasoni,&nbsp;Sandra Guidi,&nbsp;Renata Bartesaghi","doi":"10.1002/dneu.22953","DOIUrl":"10.1002/dneu.22953","url":null,"abstract":"<div>\u0000 \u0000 <p>Down syndrome (DS) is a genetic pathology characterized by various developmental defects. Unlike other clinical problems, intellectual disability is an invariant clinical trait of DS. Impairment of neurogenesis accompanied by brain hypotrophy is a typical neurodevelopmental phenotype of DS, suggesting that a reduction in the number of cells forming the brain may be a key determinant of intellectual disability. Previous evidence showed that fetuses with DS exhibit widespread hypocellularity in brain regions belonging to the temporal lobe memory systems, which may account for the typical explicit memory impairment that characterizes DS. In the current study, we have examined the basal ganglia, the insular cortex (INS), and the cingulate cortex (CCX) of fetuses with DS and age-matched controls (18–22 weeks of gestation), to establish whether cellularity defects involve regions that are not primarily involved in explicit memory. We found that fetuses with DS exhibit a notable hypocellularity in the putamen (−30%) and globus pallidus (−35%). In contrast, no cellularity differences were found in the INS and CCX, indicating that hypocellularity is not ubiquitous in the DS brain. The hypocellularity found in the basal ganglia, which are critically implicated in the control of movement, suggests that such alterations may contribute to the motor abnormalities of DS. The normal cytoarchitecture of the INS and CCX suggests that the alterations exhibited by people with DS in functions in which these regions are involved are not attributable to neuron paucity.</p>\u0000 </div>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"84 4","pages":"264-273"},"PeriodicalIF":2.7,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulation of parvalbumin expression and neurotransmitter imbalance in the auditory cortex of the BTBR mouse model of autism spectrum disorder","authors":"Binliang Tang,&nbsp;Jingting Zhao,&nbsp;Cui Zhang,&nbsp;Pengwei Qi,&nbsp;Shuyu Zheng,&nbsp;Chengyuan Xu,&nbsp;Ming Chen,&nbsp;Xiangming Ye","doi":"10.1002/dneu.22952","DOIUrl":"10.1002/dneu.22952","url":null,"abstract":"<p>Individuals diagnosed with autism spectrum disorder (ASD) frequently exhibit abnormalities in auditory perception, a phenomenon potentially attributed to alterations in the excitatory and inhibitory cells constituting cortical circuits. However, the exact genetic factors and cell types affected by ASD remain unclear. The present study investigated the balance of excitatory and inhibitory activity in the auditory cortex using BTBR T⁺ Itpr3^tf/J (BTBR) mice, a well-established model for autism research. Our investigation unveiled a reduction in parvalbumin-positive (PV⁺) neurons within the AC of BTBR mice. Remarkably, in vivo magnetic resonance spectroscopy studies disclosed an elevation in glutamate (Glu) levels alongside a decrement in γ-aminobutyric acid (GABA) levels in this cortical region. Additionally, transcriptomic analysis of the mouse model facilitated the classification of several ASD-associated genes based on their cellular function and pathways. By comparing autism risk genes with RNA transcriptome sequencing data from the ASD mouse model, we identified the recurrent target gene Scn1a and performed validation. Intriguingly, we uncovered the specific expression of Scn1a in cortical inhibitory neurons. These findings hold significant value for understanding the underlying neural mechanisms of abnormal sensory perception in animal models of ASD.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"84 4","pages":"251-263"},"PeriodicalIF":2.7,"publicationDate":"2024-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficient Dlx2-mediated astrocyte-to-neuron conversion and inhibition of neuroinflammation by NeuroD1","authors":"Min-Hui Liu,&nbsp;Yu-Ge Xu,&nbsp;Xiao-Ni Bai,&nbsp;Jian-Hua Lin,&nbsp;Zong-Qin Xiang,&nbsp;Tao Wang,&nbsp;Liang Xu,&nbsp;Gong Chen","doi":"10.1002/dneu.22951","DOIUrl":"10.1002/dneu.22951","url":null,"abstract":"<p>In vivo astrocyte-to-neuron (AtN) conversion induced by overexpression of neural transcriptional factors has great potential for neural regeneration and repair. Here, we demonstrate that a single neural transcriptional factor, Dlx2, converts mouse striatal astrocytes into neurons in a dose-dependent manner. Lineage-tracing studies in Aldh1l1-CreERT2 mice confirm that Dlx2 can convert striatal astrocytes into DARPP32⁺ and Ctip2⁺ medium spiny neurons (MSNs). Time-course studies reveal a gradual conversion from astrocytes to neurons in 1 month, with a distinct intermediate state in between astrocytes and neurons. Interestingly, when Dlx2-infected astrocytes start to lose astrocytic markers, the other local astrocytes proliferate to maintain astrocytic levels in the converted areas. Unexpectedly, although Dlx2 efficiently reprograms astrocytes into neurons in the gray matter striatum, it also induces partial reprogramming of astrocytes in the white matter corpus callosum. Such partial reprogramming of white matter astrocytes is associated with neuroinflammation, which can be suppressed by the addition of NeuroD1. Our results highlight the importance of investigating AtN conversion in both the gray matter and white matter to thoroughly evaluate therapeutic potentials. This study also unveils the critical role of anti-inflammation by NeuroD1 during AtN conversion.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"84 4","pages":"274-290"},"PeriodicalIF":2.7,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dneu.22951","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of electrostimulation and magnetic stimulation in patients with optic neuropathy: A mechanistic review","authors":"Mohammad Reza Khalili,&nbsp;Athar Shadmani,&nbsp;Fatemeh Sanie-Jahromi","doi":"10.1002/dneu.22949","DOIUrl":"10.1002/dneu.22949","url":null,"abstract":"<p>Visual impairment caused by optic neuropathies is irreversible because retinal ganglion cells (RGCs), the specialized neurons of the retina, do not have the capacity for self-renewal and self-repair. Blindness caused by optic nerve neuropathies causes extensive physical, financial, and social consequences in human societies. Recent studies on different animal models and humans have established effective strategies to prevent further RGC degeneration and replace the cells that have deteriorated. In this review, we discuss the application of electrical stimulation (ES) and magnetic field stimulation (MFS) in optic neuropathies, their mechanisms of action, their advantages, and limitations. ES and MFS can be applied effectively in the field of neuroregeneration. Although stem cells are becoming a promising approach for regenerating RGCs, the inhibitory environment of the CNS and the long visual pathway from the optic nerve to the superior colliculus are critical barriers to overcome. Scientific evidence has shown that adjuvant treatments, such as the application of ES and MFS help direct thetransplanted RGCs to extend their axons and form new synapses in the central nervous system (CNS). In addition, these techniques improve CNS neuroplasticity and decrease the inhibitory effects of the CNS. Possible mechanisms mediating the effects of electrical current on biological tissues include the release of anti-inflammatory cytokines, improvement of microcirculation, stimulation of cell metabolism, and modification of stem cell function. ES and MFS have the potential to promote angiogenesis, direct axon growth toward the intended target, and enhance appropriate synaptogenesis in optic nerve regeneration.</p>","PeriodicalId":11300,"journal":{"name":"Developmental Neurobiology","volume":"84 3","pages":"236-248"},"PeriodicalIF":2.7,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}