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This research topic was suggested by Robert Sachdev to bring together a series of articles dealing with the laminar organization of the neocortex. By convention, there are six cortical layers but this number may vary throughout the cerebral cortex of a given species or between species: many regions lack one or more layers, whereas in other regions there are more than six layers. The laminar location of cortical neurons —their cell bodies— is determined during development. However, neurons are more than their cell bodies; they also have dendrites that may span within a given layer (intralaminar neurons) or across a variety of layers (translaminar neurons). For example, layer V pyramidal neurons have dendrites that span the entire cortical depth, whereas layer III pyramidal neurons have dendrites that span across layers I to IV. Some GABAergic interneurons have dendrites located within a cortical layer (e.g., neurogliaform cells), whereas the dendrites of other interneurons span several layers (e.g., bitufted cells). For neurons having dendrites that cross laminar boundaries, one might ask, why segregate their cell bodies so carefully into lamina? Among many other obvious questions: What is the evidence for or against integration of information across laminae for neurons whose dendrites span several layers? A traditional view is that activity flows through cortical layers in a feed-forward manner, going from layer IV, to layers II and III and onwards. Another view is that cortical layers can have distinct inputs that activate them, triggering spikes. Can processing sequences be state dependent? Furthermore, different cortical layers have distinct transcriptomic profiles, neurochemical attributes, connectivity patterns, number and types of synapses and many other structural attributes. Thus, based on anatomy, or physiology or imaging: What is the function of each cortical layer? What do the different layers do?

periallocortex --- receptors --- cell types --- GABAergic connectivity --- isocortex --- insular cortex --- olfactory --- Reeler --- Pyramidal neurons --- Cortical evolution

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The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimer's disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders.

Neurons --- neuronal migration --- Schizophrenia --- Depression --- Neuronal Death --- Reeler --- Synapses --- autism --- intracellular pathways

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The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimer's disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders.

Neurons --- neuronal migration --- Schizophrenia --- Depression --- Neuronal Death --- Reeler --- Synapses --- autism --- intracellular pathways

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A revelatory tale of how the human brain develops, from conception to birth and beyondBy the time a baby is born, its brain is equipped with billions of intricately crafted neurons wired together through trillions of interconnections to form a compact and breathtakingly efficient supercomputer. Zero to Birth takes you on an extraordinary journey to the very edge of creation, from the moment of an egg’s fertilization through each step of a human brain’s development in the womb—and even a little beyond.As pioneering experimental neurobiologist W. A. Harris guides you through the process of how the brain is built, he takes up the biggest questions that scientists have asked about the developing brain, describing many of the thrilling discoveries that were foundational to our current understanding. He weaves in a remarkable evolutionary story that begins billions of years ago in the Proterozoic eon, when multicellular animals first emerged from single-cell organisms, and reveals how the growth of a fetal brain over nine months reflects the brain’s evolution through the ages. Our brains have much in common with those of other animals, and Harris offers an illuminating look at how comparative animal studies have been crucial to understanding what makes a human brain human.An unforgettable chronicle of one of nature’s greatest achievements, Zero to Birth describes how the brain’s incredible feat of orchestrated growth ensures that every brain is unique, and how breakthroughs at the frontiers of science are helping us to decode many traits that only reveal themselves later in life.

SCIENCE / Life Sciences / Neuroscience. --- Action potential. --- Agrin. --- Angiogenesis. --- Antibody. --- Apoptosis. --- Astrocyte. --- Axon guidance. --- Axon. --- Blastula. --- Brain asymmetry. --- Broca's area. --- Cancer cell. --- Cell type. --- Cerebral atrophy. --- Cerebral cortex. --- Charles Darwin. --- Chemical synapse. --- Critical period. --- Cyclopamine. --- Degenerative disease. --- Dendrite. --- Down syndrome. --- Ectoderm. --- Embryo. --- Embryology. --- Endocrinology. --- Eric Knudsen. --- Evolution. --- FOXP2. --- Filopodia. --- Forebrain. --- Ganglion cell. --- Gastrulation. --- Gene. --- Growth cone. --- Hans Spemann. --- Hebbian theory. --- Hindbrain. --- Hirschsprung's disease. --- Homeosis. --- Hox gene. --- Human brain. --- Immortalised cell line. --- John Gurdon. --- Lancelot Hogben. --- Lateralization of brain function. --- Marian Diamond. --- Midbrain. --- Model organism. --- Morphogen. --- Motor neuron. --- Muscle. --- Myocyte. --- Nematode. --- Nervous tissue. --- Neural crest. --- Neural development. --- Neural plate. --- Neural stem cell. --- Neural tube defect. --- Neural tube. --- Neuroblast. --- Neuroblastoma. --- Neuroepithelial cell. --- Neuroglia. --- Neuroimaging. --- Neuron doctrine. --- Neuron. --- Organoid. --- Petri dish. --- Progenitor cell. --- Proneural genes. --- Protein. --- Protocadherin. --- Purkinje cell. --- Reeler. --- Reelin. --- Renshaw cell. --- Reticular theory. --- Retinoic acid. --- Roel Nusse. --- Ross Granville Harrison. --- Sarcoma. --- Sonic hedgehog. --- Spina bifida. --- Spinal cord. --- Spindle apparatus. --- Stem cell. --- Sydney Brenner. --- Synapsis. --- Synaptic plasticity. --- Thomas Hunt Morgan. --- Thrombospondin. --- Torsten Wiesel. --- Transformation (genetics). --- Twin. --- Vertebrate. --- Visual word form area. --- White blood cell. --- Zygote. --- Brain --- Growth. --- Neuronal Plasticity --- SCIENCE / Life Sciences / Neuroscience --- SCIENCE / Life Sciences / Developmental Biology --- growth & development --- embryology --- physiology