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"neuronal development"
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Extracellular matrix and biomimetic engineering microenvironment for neuronal differentiation
Extracellular matrix (ECM) influences cell differentiation through its structural and biochemical properties. In nervous system, neuronal behavior is influenced by these ECMs structures which are present in a meshwork, fibrous, or tubular forms encompassing specific molecular compositions. In addition to contact guidance, ECM composition and structures also exert its effect on neuronal differentiation. This short report reviewed the native ECM structure and composition in central nervous system and peripheral nervous system, and their impact on neural regeneration and neuronal differentiation. Using topographies, stem cells have been differentiated to neurons. Further, focussing on engineered biomimicking topographies, we highlighted the role of anisotropic topographies in stem cell differentiation to neurons and its recent temporal application for efficient neuronal differentiation.
Journal Article
Pathophysiological Mechanisms in Neurodevelopmental Disorders Caused by Rac GTPases Dysregulation: What’s behind Neuro-RACopathies
Rho family guanosine triphosphatases (GTPases) regulate cellular signaling and cytoskeletal dynamics, playing a pivotal role in cell adhesion, migration, and cell cycle progression. The Rac subfamily of Rho GTPases consists of three highly homologous proteins, Rac 1–3. The proper function of Rac1 and Rac3, and their correct interaction with guanine nucleotide-exchange factors (GEFs) and GTPase-activating proteins (GAPs) are crucial for neural development. Pathogenic variants affecting these delicate biological processes are implicated in different medical conditions in humans, primarily neurodevelopmental disorders (NDDs). In addition to a direct deleterious effect produced by genetic variants in the RAC genes, a dysregulated GTPase activity resulting from an abnormal function of GEFs and GAPs has been involved in the pathogenesis of distinctive emerging conditions. In this study, we reviewed the current pertinent literature on Rac-related disorders with a primary neurological involvement, providing an overview of the current knowledge on the pathophysiological mechanisms involved in the neuro-RACopathies.
Journal Article
Zero to birth : how the human brain is built
\"By the time a baby is born, its brain has nearly 100 billion intricately shaped neurons wired together to comprise a small, soft-matter supercomputer. How is this incredibly complicated organ built in just nine months? This book is a step-by-step guide to what we know about the development of the human brain, from its earliest embryonic origin to birth and a little beyond. Written from an experimental neuroscientist's perspective, this book provides readers with a conceptual understanding of the field of developmental neurobiology, outlining both the biological mechanisms (genetic, environmental, and stochastic) that play significant and interrelated roles in neural development, and how we have come to understand the human brain's construction and function. Highlighting the major questions that have propelled the field forward - including those pushing at the frontiers of the field today - and the stories of major discoveries made by pioneering scientists around the world, the book describes how the structures and mechanisms of the developing brain were discovered. Chapters progress chronologically, tracking the actual growth and development of the human brain from conception to just after birth, as well as the history of how these mechanisms were revealed. Throughout, findings from studies of model organisms, such as nematodes, flies, frogs, fish, birds, mice, and sometimes non-human primates, are woven into the narrative and put into the context of a human embryo or fetus, as there are clear indications that the same processes involving the same genes are found across species. The book concludes with a discussion of what makes individual brains unique and how research on early neural development is helping us better understand the genetic and embryonic origins of many neurological and cognitive traits that only reveal themselves later in life\"-- Provided by publisher.
Book
Combined frontal and parietal P300 amplitudes indicate compensated cognitive processing across the lifespan
In the present study the frontal and parietal P300, elicited in an auditory oddball paradigm were investigated in a large sample of healthy participants (N = 1572), aged 6-87. According to the concepts of the compensation-related utilization of neural circuits hypothesis (CRUNCH) it was hypothesized that the developmental trajectories of the frontal P300 would reach a maximum in amplitude at an older age than the amplitude of the parietal P300 amplitude. In addition, the amplitude of the frontal P300 was expected to increase with aging in adulthood in contrast to a decline in amplitude of the parietal P300 amplitude. Using curve-fitting methods, a comparison was made between the developmental trajectories of the amplitudes of the frontal and parietal P300. It was found that the developmental trajectories of frontal and parietal P300 amplitudes differed significantly across the lifespan. During adulthood, the amplitude of the parietal P300 declines with age, whereas both the frontal P300 amplitude and behavioral performance remain unaffected. A lifespan trajectory of combined frontal and parietal P300 amplitudes was found to closely resemble the lifespan trajectory of behavioral performance. Our results can be understood within the concepts of CRUNCH. That is, to compensate for declining neural resources, older participants recruit additional neural resources of prefrontal origin and consequently preserve a stable behavioral performance. Though, a direct relation between amplitude of the frontal P300 and compensatory mechanisms cannot yet be claimed.
Journal Article
Efficient simulation of neural development using shared memory parallelization
The Neural Development Simulator, NeuroDevSim, is a Python module that simulates the most important aspects of brain development: morphological growth, migration, and pruning. It uses an agent-based modeling approach inherited from the NeuroMaC software. Each cycle has agents called fronts execute model-specific code. In the case of a growing dendritic or axonal front, this will be a choice between extension, branching, or growth termination. Somatic fronts can migrate to new positions and any front can be retracted to prune parts of neurons. Collision detection prevents new or migrating fronts from overlapping with existing ones. NeuroDevSim is a multi-core program that uses an innovative shared memory approach to achieve parallel processing without messaging. We demonstrate linear strong parallel scaling up to 96 cores for large models and have run these successfully on 128 cores. Most of the shared memory parallelism is achieved without memory locking. Instead, cores have only write privileges to private sections of arrays, while being able to read the entire shared array. Memory conflicts are avoided by a coding rule that allows only active fronts to use methods that need writing access. The exception is collision detection, which is needed to avoid the growth of physically overlapping structures. For collision detection, a memory-locking mechanism was necessary to control access to grid points that register the location of nearby fronts. A custom approach using a serialized lock broker was able to manage both read and write locking. NeuroDevSim allows easy modeling of most aspects of neural development for models simulating a few complex or thousands of simple neurons or a mixture of both.
Journal Article
GM1 Ganglioside Is A Key Factor in Maintaining the Mammalian Neuronal Functions Avoiding Neurodegeneration
Many species of ganglioside GM1, differing for the sialic acid and ceramide content, have been characterized and their physico-chemical properties have been studied in detail since 1963. Scientists were immediately attracted to the GM1 molecule and have carried on an ever-increasing number of studies to understand its binding properties and its neurotrophic and neuroprotective role. GM1 displays a well balanced amphiphilic behavior that allows to establish strong both hydrophobic and hydrophilic interactions. The peculiar structure of GM1 reduces the fluidity of the plasma membrane which implies a retention and enrichment of the ganglioside in specific membrane domains called lipid rafts. The dynamism of the GM1 oligosaccharide head allows it to assume different conformations and, in this way, to interact through hydrogen or ionic bonds with a wide range of membrane receptors as well as with extracellular ligands. After more than 60 years of studies, it is a milestone that GM1 is one of the main actors in determining the neuronal functions that allows humans to have an intellectual life. The progressive reduction of its biosynthesis along the lifespan is being considered as one of the causes underlying neuronal loss in aged people and severe neuronal decline in neurodegenerative diseases. In this review, we report on the main knowledge on ganglioside GM1, with an emphasis on the recent discoveries about its bioactive component.
Journal Article
Exosomes regulate neurogenesis and circuit assembly
Exosomes are thought to be released by all cells in the body and to be involved in intercellular communication. We tested whether neural exosomes can regulate the development of neural circuits. We show that exosome treatment increases proliferation in developing neural cultures and in vivo in dentate gyrus of P4 mouse brain. We compared the protein cargo and signaling bioactivity of exosomes released by hiPSC-derived neural cultures lacking MECP2, a model of the neurodevelopmental disorder Rett syndrome, with exosomes released by isogenic rescue control neural cultures. Quantitative proteomic analysis indicates that control exosomes contain multiple functional signaling networks known to be important for neuronal circuit development. Treating MECP2-knockdown human primary neural cultures with control exosomes rescues deficits in neuronal proliferation, differentiation, synaptogenesis, and synchronized firing, whereas exosomes from MECP2-deficient hiPSC neural cultures lack this capability. These data indicate that exosomes carry signaling information required to regulate neural circuit development.
Journal Article
Two-dimensional Ti3C2Tx MXene promotes electrophysiological maturation of neural circuits
Background
The ideal neural interface or scaffold for stem cell therapy shall have good biocompatibility promoting survival, maturation and integration of neural stem cells (NSCs) in targeted brain regions. The unique electrical, hydrophilic and surface-modifiable properties of Ti
3
C
2
T
x
MXene make it an attractive substrate, but little is known about how it interacts with NSCs during development and maturation.
Results
In this study, we cultured NSCs on Ti
3
C
2
T
x
MXene and examined its effects on morphological and electrophysiological properties of NSC-derived neurons. With a combination of immunostaining and patch-clamp recording, we found that Ti
3
C
2
T
x
MXene promotes NSCs differentiation and neurite growth, increases voltage-gated current of Ca
2+
but not Na
+
or K
+
in matured neurons, boosts their spiking without changing their passive membrane properties, and enhances synaptic transmission between them.
Conclusions
These results expand our understanding of interaction between Ti
3
C
2
T
x
MXene and NSCs and provide a critical line of evidence for using Ti
3
C
2
T
x
MXene in neural interface or scaffold in stem cell therapy.
Journal Article