scholarly journals Eph-ephrin signaling in nervous system development

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 413 ◽  
Author(s):  
Karina S. Cramer ◽  
Ilona J. Miko
Keyword(s):  
Nervous System ◽  
Signaling Pathways ◽  
Neuronal Migration ◽  
System Development ◽  
Nervous System Development ◽  
Eph Receptors ◽  
Binding Affinities ◽  
Developmental Processes ◽  
Axon Targeting

Ephrins and Eph receptors enable contact-mediated interactions between cells at every stage of nervous system development. In spite of their broad binding affinities, Eph proteins facilitate specificity in neuronal migration and axon targeting. This review focuses on recent studies that demonstrate how these proteins interact with each other, and with other signaling pathways, to guide specificity in a diverse set of developmental processes.

scholarly journals Dramatic neurological and biological effects by Botulinum Neurotoxin Type A on SH-SY5Y neuroblastoma cells, beyond the blockade of neurotransmitter release

2020 ◽  
Author(s):  
Lei Wang ◽  
Carol S. Ringelberg ◽  
Bal R. Singh
Keyword(s):  
Nervous System ◽  
Signaling Pathways ◽  
Neurotransmitter Release ◽  
Site Effects ◽  
Botulinum Neurotoxin ◽  
System Development ◽  
Neuroblastoma Cells ◽  
Type A ◽  
Nervous System Development ◽  
Time Points

Abstract Background Gene expression profile analysis on mammalian cell lines and animal models after exposure to botulinum neurotoxin (BoNT) have been investigated in several studies in recent years. This provides a powerful tool to identify critical signaling pathways involved in the biological and inflammatory responses to BoNT and helps to determine the mechanism of the function of botulinum toxins. One of the key clinical characteristics of BoNT is its prolonged on-site effects. The role of BoNT on the blockage of neurotransmitter acetylcholine release in the neuromuscular junction has been well established. However, the effects of the treatment time of BoNT on the human cellular model and its potential mechanism remain to be defined. This study is aimed to use the gene microarray technology to compare the two physiological critical time points of BoNT type A (BoNT/A) treatment of human neuroblastoma cells and to advance our understanding of the profound biological influences that toxin molecules play in the neuronal cellular system. Results SH-SY5Y cells were treated with BoNT/A for 4 and 48 hours which represent the time needed for the entrance of toxin into the cells and the time necessary for the initial appearance of the on-site effects after BoNT application. A comparison of the two time points identified 122 functional groups that are significantly changed. The top five groups are the alternative splicing, phosphoprotein, nucleus, cytoplasm, and acetylation. Furthermore, after 48 hours there were 744 genes significantly up-regulated and 624 genes significantly down-regulated (p‹ 0.01). These genes fell into the following neurological and biological annotation groups: Nervous system development, proteinaceous extracellular matrix, signaling pathways regulating pluripotency of stem cells, cellular function and signal transduction, and apoptosis. We have also noticed that the up-regulated groups contained neuronal cell development, nervous system development, and metabolic processes while the down-regulated groups contained many chromosomes and cell cycle categories. Conclusions The effects of BoNT/A on neuronal cells extend beyond blocking the neurotransmitter release, and that BoNT/A is a multifunctional molecule that can evoke profound cellular responses which warrant a more in-depth understanding of the mechanism of the toxin’s effects after administration.

Comparative Milestones in Rodent and Human Postnatal Central Nervous System Development

2021 ◽  
pp. 019262332110469
Author(s):  
Caroline J. Zeiss
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Postnatal Development ◽  
System Development ◽  
Nervous System Development ◽  
Developmental Processes ◽  
Neurodevelopmental Toxicity ◽  
Mole Rat ◽  
Developmental Rates ◽  
Development Methods

Within the substantially different time scales characterizing human and rodent brain development, key developmental processes are remarkably preserved. Shared processes include neurogenesis, myelination, synaptogenesis, and neuronal and synaptic pruning. In general, altricial rodents experience greater central nervous system (CNS) immaturity at birth and accelerated postnatal development compared to humans, in which protracted development of certain processes such as neocortical myelination and synaptic maturation extend into adulthood. Within this generalization, differences in developmental rates of various structures must be understood to accurately model human neurodevelopmental toxicity in rodents. Examples include greater postnatal neurogenesis in rodents, particularly within the dentate gyrus of rats, ongoing generation of neurons in the rodent olfactory bulb, differing time lines of neurotransmitter maturation, and differing time lines of cerebellar development. Comparisons are made to the precocial guinea pig and the long-lived naked mole rat, which, like primates, experiences more advanced CNS development at birth, with more protracted postnatal development. Methods to study various developmental processes are summarized using examples of comparative postnatal injury in humans and rodents.

scholarly journals TheC. elegansephrin EFN-4 functions non-cell autonomously with heparan sulfate proteoglycans to promote axon outgrowth and branching

2015 ◽  
Author(s):  
Alicia A Schwieterman ◽  
Alyse N Steves ◽  
Vivian Yee ◽  
Cory J Donelson ◽  
Aaron Pital ◽  
...  
Keyword(s):  
Nervous System ◽  
Neurite Outgrowth ◽  
Motor Neurons ◽  
System Development ◽  
Nervous System Development ◽  
The Body ◽  
Tissue Type ◽  
Eph Receptors ◽  
C Elegans ◽  
Core Proteins

The Eph receptors and their cognate ephrin ligands play key roles in many aspects of nervous system development. These interactions typically occur within an individual tissue type, serving either to guide axons to their terminal targets or to define boundaries between the rhombomeres of the hindbrain. We have identified a novel role for theCaenorhabditis elegansephrin EFN-4 in promoting primary neurite outgrowth in AIY interneurons and D-class motor neurons. Rescue experiments reveal that EFN-4 functions non-cell autonomously in the epidermis to promote primary neurite outgrowth. We also find that EFN-4 plays a role in promoting ectopic axon branching in aC. elegansmodel of X-linked Kallmann syndrome. In this context, EFN-4 functions non-cell autonomously in the body wall muscle, and in parallel with HS biosynthesis genes and HSPG core proteins, which function cell autonomously in the AIY neurons. This is the first report of an epidermal ephrin providing a developmental cue to the nervous system.

scholarly journals Dramatic neurological and biological effects by Botulinum Neurotoxin Type A on SH-SY5Y neuroblastoma cells, beyond the blockade of neurotransmitter release

2020 ◽  
Author(s):  
Lei Wang ◽  
Carol S. Ringelberg ◽  
Bal R. Singh
Keyword(s):  
Nervous System ◽  
Signaling Pathways ◽  
Neurotransmitter Release ◽  
Site Effects ◽  
Botulinum Neurotoxin ◽  
System Development ◽  
Neuroblastoma Cells ◽  
Type A ◽  
Nervous System Development ◽  
Time Points

Abstract Background Gene expression profile analysis on mammalian cell lines and animal models after exposure to botulinum neurotoxin (BoNT) have been investigated in several studies in recent years. This provides a powerful tool to identify critical signaling pathways involved in the biological and inflammatory responses to BoNT and helps to determine the mechanism of the function of botulinum toxins. One of the key clinical characteristics of BoNT is its prolonged on-site effects. The role of BoNT on the blockage of neurotransmitter acetylcholine release in the neuromuscular junction has been well established. However, the effects of the treatment time of BoNT on the human cellular model and its potential mechanism remain to be defined. This study is aimed to use the gene microarray technology to compare the two physiological critical time points of BoNT type A (BoNT/A) treatment of human neuroblastoma cells and to advance our understanding of the profound biological influences that toxin molecules play in the neuronal cellular system. Results SH-SY5Y cells were treated with BoNT/A for 4 and 48 hours which represent the time needed for the entrance of toxin into the cells and the time necessary for the initial appearance of the on-site effects after BoNT application. A comparison of the two time points identified 122 functional groups that are significantly changed. The top five groups are the alternative splicing, phosphoprotein, nucleus, cytoplasm, and acetylation. Furthermore, after 48 hours there were 744 genes significantly up-regulated and 624 genes significantly down-regulated (p‹ 0.01). These genes fell into the following neurological and biological annotation groups: Nervous system development, proteinaceous extracellular matrix, signaling pathways regulating pluripotency of stem cells, cellular function and signal transduction, and apoptosis. We have also noticed that the up-regulated groups contained neuronal cell development, nervous system development, and metabolic processes while the down-regulated groups contained many chromosomes and cell cycle categories. Conclusions The effects of BoNT/A on neuronal cells extend beyond blocking the neurotransmitter release, and that BoNT/A is a multifunctional molecule that can evoke profound cellular responses which warrant a more in-depth understanding of the mechanism of the toxin’s effects after administration.

Antenatal Glucocorticoids Supplementation and Central Nervous System Development

2013 ◽  
Vol 14 (2) ◽  
pp. 160-166
Author(s):  
Diego Gazzolo ◽  
Laura D. Serpero ◽  
Alessandro Frigiola ◽  
Raul Abella ◽  
Alessandro Giamberti ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
Central Nervous System Development

scholarly journals Incorporation of 5-Bromo-2′-deoxyuridine into DNA and Proliferative Behavior of Cerebellar Neuroblasts: All That Glitters Is Not Gold

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1453
Author(s):  
Joaquín Martí-Clúa
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
System Development ◽  
Nervous System Development ◽  
Current Data ◽  
Cellular Mechanisms ◽  
Dividing Cells ◽  
The Central Nervous System ◽  
Repeated Doses ◽  
Pyrimidine Analog

The synthetic halogenated pyrimidine analog, 5-bromo-2′-deoxyuridine (BrdU), is a marker of DNA synthesis. This exogenous nucleoside has generated important insights into the cellular mechanisms of the central nervous system development in a variety of animals including insects, birds, and mammals. Despite this, the detrimental effects of the incorporation of BrdU into DNA on proliferation and viability of different types of cells has been frequently neglected. This review will summarize and present the effects of a pulse of BrdU, at doses ranging from 25 to 300 µg/g, or repeated injections. The latter, following the method of the progressively delayed labeling comprehensive procedure. The prenatal and perinatal development of the cerebellum are studied. These current data have implications for the interpretation of the results obtained by this marker as an index of the generation, migration, and settled pattern of neurons in the developing central nervous system. Caution should be exercised when interpreting the results obtained using BrdU. This is particularly important when high or repeated doses of this agent are injected. I hope that this review sheds light on the effects of this toxic maker. It may be used as a reference for toxicologists and neurobiologists given the broad use of 5-bromo-2′-deoxyuridine to label dividing cells.

Editorial overview: Microtubules in nervous system development

2021 ◽  
Vol 81 (3) ◽  
pp. 229-230
Author(s):  
Frank Bradke ◽  
Antonina Roll‐Mecak
Keyword(s):  
Nervous System ◽  
System Development ◽  
Nervous System Development
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