发育神经生物学（前身为《神经生物学杂志》）发表关于神经系统发育、再生、修复和可塑性以及行为个体发育的原创研究文章。征集这些领域的高质量贡献，强调实验而不是纯粹的描述性工作。该杂志还将考虑报告用于研究神经系统发育的新方法和技术的手稿，以及关于当前重要主题的偶尔特刊。我们欢迎读者就可能的主题提出建议。

Developmental Neurobiology is a scholarly journal focused on original research articles concerning the development, regeneration, repair, and plasticity of the nervous system, as well as the developmental behavior of individuals (formerly known as the Journal of Neurobiology). We welcome high-quality contributions in these areas, emphasizing experimental work over purely descriptive studies. The journal also considers manuscripts reporting new methods and techniques for researching nervous system development, as well as occasional special issues on current important topics. We encourage readers to suggest potential themes.

《Developmental Neurobiology》是一本专注于神经系统发育、再生、修复和可塑性以及行为个体发育的学术期刊（前身为《神经生物学杂志》）。我们欢迎在这些领域内的高质量原创研究文章，特别强调实验研究而非纯描述性工作。此外，本期刊也会考虑关于神经系统发育的新方法和技术的报告，以及偶尔发布关于当前重要主题的特刊。我们鼓励读者提出可能的主题建议。

Developmental Neurobiology

Abstract Motor neuron disease (MND), including amyotrophic lateral sclerosis, spinal muscular atrophy and others, involved the upper or lower motor neurons selective loss, is characterized by neurodegeneration and neuroinflammation, in conjunction with microglia. We summarized that pathways and key mediators are associated with microglia, such as fractalkine signaling, purinergic signaling, NF‐κB signaling, p38 MAPK signaling, TREM2‐APOE signaling, ROCK signaling, C1q signaling, and Ion channel, which are involved in the activation, proliferation, and inflammation of microglia. This review aims to identify the microglia‐related molecular target and explore potential treatment strategies for MND based on that target.

Min‐Jia Wang

Lu Kang

Yao‐Zheng Wang

Bi‐Ru Yang

Chun Zhang

Yu‐Feng Lu

Liang Kang

Microglia in motor neuron disease: Signaling evidence from last 10 years

运动神经元疾病中的小胶质细胞：过去十年中的信号证据

ABSTRACT Social impairment is one of the major symptoms in multiple psychiatric disorders, including autism spectrum disorder (ASD). Accumulated studies indicate a crucial role for the gut microbiota in social development, but these mechanisms remain unclear. This review focuses on two strategies adopted to elucidate the complicated relationship between gut bacteria and host social behavior. In a top‐down approach, researchers have attempted to correlate behavioral abnormalities with altered gut microbial profiles in rodent models of ASD, including BTBR mice, maternal immune activation (MIA), maternal valproic acid (VPA) and maternal high‐fat diet (MHFD) offspring. In a bottom‐up approach, researchers use germ‐free (GF) animals, antibiotics, probiotics or pathogens to manipulate the intestinal environment and ascertain effects on social behavior. The combination of both approaches will hopefully pinpoint specific bacterial communities that control host social behavior. Further discussion of how brain development and circuitry is impacted by depletion of gut microbiota is also included. The converging evidence strongly suggests that gut microbes affect host social behavior through the alteration of brain neural circuits. Investigation of intestinal microbiota and host social behavior will unveil any bidirectional communication between the gut and brain and provide alternative therapeutic targets for ASD. © 2018 Wiley Periodicals, Inc. Develop Neurobiol 78: 474–499, 2018

Brittany D. Needham

Weiyi Tang

Wei‐Li Wu

Searching for the gut microbial contributing factors to social behavior in rodent models of autism spectrum disorder

寻找自闭症谱系障碍啮齿动物模型中肠道微生物对社会行为贡献因素的研究

Melanopsin ganglion cells express the photopigment melanopsin and are the first functional photoreceptors to develop in the mammalian retina. They have been shown to play a variety of important roles in visual development and behavior in the early postnatal period (Johnson et al., 2010; Kirkby and Feller, 2013; Rao et al., 2013; Renna et al., 2011). Here, we probed the maturation of the dendritic arbors of melanopsin ganglion cells during this developmental period in mice. We found that some melanopsin ganglion cells (mainly the M1‐subtype) transiently extend their dendrites not only into the inner plexiform layer (where they receive synaptic inputs from bipolar and amacrine cells) but also into the outer plexiform layer, where in mature retina, rod and cone photoreceptors are thought to contact only bipolar and horizontal cells. Thus, some immature melanopsin ganglion cells are biplexiform. This feature is much less common although still present in the mature retina. It reaches peak incidence 8–12 days after birth, before the eyes open and bipolar cells are sufficiently mature to link rods and cones to ganglion cells. At this age, some outer dendrites of melanopsin ganglion cells lie in close apposition to the axon terminals of cone photoreceptors and express a postsynaptic marker of glutamatergic transmission, postsynaptic density‐95 protein (PSD‐95). These findings raise the possibility of direct, monosynaptic connections between cones and melanopsin ganglion cells in the early postnatal retina. We provide a detailed description of the developmental profile of these processes and consider their possible functional and evolutionary significance. © 2015 Wiley Periodicals, Inc. Develop Neurobiol 75: 935–946, 2015

Jordan M. Renna

Deepa K. Chellappa

Christopher L. Ross

Maureen E. Stabio

David M. Berson

Devel Neurobio

Melanopsin ganglion cells extend dendrites into the outer retina during early postnatal development

黑视蛋白神经节细胞在出生后早期发育中向外视网膜延伸树突

ABSTRACT Growth differentiation factor 15 (GDF15) can be induced under various stress conditions. This study aimed to explore the role of GDF15 in oxygen‐glucose deprivation/reoxygenation (OGD/R)‐induced HT22 cells. OGD/R was employed to induce the HT22 cell model, and GDF15 expression was upregulated via transfection. Subsequently, the effects on inflammatory factors, oxidative stress markers, apoptosis‐related proteins, and ferroptosis markers were detected. Relevant indicators were evaluated using techniques such as ELISA, probes, flow cytometry, and western blotting. Furthermore, changes in these phenotypes under the influence of the endoplasmic reticulum (ER) stress agonist tunicamycin (TM) were evaluated. The result showed that GDF15 was significantly up‐regulated in OGD/R‐treated HT22 cells. Overexpression of GDF15 significantly reduced the levels of inflammatory factors tumor necrosis factor‐α, IL (interleukin)‐1β, and IL‐6, inhibited the production of reactive oxygen species and MDA, and improved activity of superoxide dismutase and GSH‐Px. Flow cytometry and western blotting results showed that GDF15 overexpression significantly reduced cell apoptosis, reduced caspase3 activity, and regulated the expression of Bcl2 and Bax. In addition, overexpression of GDF15 reduces the levels of ferroptosis markers by inhibiting ER stress. ER stress inducer TM can reverse the protective effects of GDF15 overexpression and promote inflammation, oxidative stress, and apoptosis. This study shows that overexpression of GDF15 reduces OGD/R‐induced HT22 cell damage, and ER stress‐mediated ferroptosis is included in the regulatory mechanisms. This provides a theoretical basis for GDF15 as a new target for the treatment of cerebral ischemia‐reperfusion injury.

Haiming Li

Bin Chen

Zhelin Chen

Jianming Luo

Binyuan Yang

Overexpression of Growth Differentiation Factor 15 Reduces Neuronal Cell Damage Induced by Oxygen‐Glucose Deprivation/Reoxygenation via Inhibiting Endoplasmic Reticulum Stress‐Mediated Ferroptosis

过表达生长分化因子15通过抑制内质网应激介导的铁死亡减轻氧糖剥夺/再灌注诱导的神经元细胞损伤

ABSTRACT 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, chrna3 , chrnb4 , and chrna5 , 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 chrna3 tdTomato , chrnb4 eGFP , and chrna5 tdTomato in the intestinal enteric nervous system; chrna5 tdTomato and chrnb4 eGFP in sensory ganglia of the lateral line; and chrnb4 eGFP in the ear. In the CNS, the expression of chrnb4 eGFP and chrna5 tdTomato was found in the retina, all three expressed in diverse regions of the brain, where a portion of chrna3 tdTomato and chrnb4 eGFP cells were found to be inhibitory efferent neurons projecting to the lateral line. Within the spinal cord, we identify distinct populations of chrna3 tdTomato ‐, chrnb4 eGFP ‐, and chrna5 tdTomato ‐expressing neurons within the locomotor network, including dmrt3a ‐expressing interneurons and mnx1 ‐expressing motor neurons. Notably, three to four primary motor neurons per hemisegment were labeled by both chrna3 tdTomato and chrnb4 eGFP . Interestingly, we identified an sl‐type secondary motor neuron per hemisegement that strongly expressed chrna5 tdTomato and co‐expressed chrnb4 eGFP . 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.

Yuanqi Hua

Judith Habicher

Matthias Carl

Remy Manuel

Henrik Boije

Novel Transgenic Zebrafish Lines to Study the CHRNA3‐B4‐A5 Gene Cluster

新型转基因斑马鱼品系用于研究CHRNA3‐B4‐A5基因簇

ABSTRACT 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.

Ziyao Han

Xiaoyue Yang

Jianxiong Gui

Hanyu Luo

Dishu Huang

Hengsheng Chen

Li Cheng

Ping Yuan

Li Jiang

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

海马初级纤毛功能缺陷及LKB1/AMPK信号通路异常与高龄产妇后代自噬活性抑制相关

ABSTRACT 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. Summary : 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.

Maiara de Aguiar da Costa

Gustavo Zanette Fernandes

Eduarda Maiochi

Maria Fernanda Pedro Ebs

Flávia da Silva Darós

Sofia Januário Bolan

Rosiane Ronchi Nascimento Costa

Victória Linden de Rezende

Gláucia Crispim da Silva

Rafael Mariano Bitencourt

Cinara Ludvig Gonçalves

Effects of Cannabidiol Isolated or in Association With Risperidone in an Animal Model of Autism

动物模型中自闭症大麻二酚单独或与利培酮联合使用的效果

ABSTRACT 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.

Marco Emili

Fiorenza Stagni

Maria Paola Bonasoni

Sandra Guidi

Renata Bartesaghi

Cellularity Defects Are Not Ubiquitous in the Brains of Fetuses With Down Syndrome

胎儿唐氏综合症大脑中细胞缺陷并非普遍存在

Abbreviation	Dev. Neurobiol.
Journal Impact	2.74
Quartiles(Global)	NEUROSCIENCES(Q3)

ISSN	1932-8451, 1932-846X
h-index	141

Publication Information	Publisher: John Wiley & Sons Inc.，Publishing cycle: Monthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 2007，Proportion of original research papers: 69.70%，Self Citation Rate:0.00%， Gold OA Rate: 34.00%
Average review cycle	网友分享经验：偏慢,4-8周
Average recruitment ratio	网友分享经验：一般

Developmental Neurobiology

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Microglia in motor neuron disease: Signaling evidence from last 10 years

Searching for the gut microbial contributing factors to social behavior in rodent models of autism spectrum disorder

Melanopsin ganglion cells extend dendrites into the outer retina during early postnatal development

Overexpression of Growth Differentiation Factor 15 Reduces Neuronal Cell Damage Induced by Oxygen‐Glucose Deprivation/Reoxygenation via Inhibiting Endoplasmic Reticulum Stress‐Mediated Ferroptosis

Novel Transgenic Zebrafish Lines to Study the CHRNA3‐B4‐A5 Gene Cluster

Overexpression of Growth Differentiation Factor 15 Reduces Neuronal Cell Damage Induced by Oxygen‐Glucose Deprivation/Reoxygenation via Inhibiting Endoplasmic Reticulum Stress‐Mediated Ferroptosis

Novel Transgenic Zebrafish Lines to Study the CHRNA3‐B4‐A5 Gene Cluster

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

Effects of Cannabidiol Isolated or in Association With Risperidone in an Animal Model of Autism

Cellularity Defects Are Not Ubiquitous in the Brains of Fetuses With Down Syndrome