Normal and abnormal neuronal migration in the developing cerebral cortex.
Neuronal migration is the critical cellular process which initiates histogenesis of cerebral cortex. Migration involves a series of complex cell interactions and transformation. After completing their final mitosis, neurons migrate from the ventricular zone into the cortical plate, and then establish neuronal lamina and settle onto the outermost layer, forming an "inside-out" gradient of maturation. This process is guided by radial glial fibers, requires proper receptors, ligands, other unknown extracellular factors, and local signaling to stop neuronal migration. This process is also highly sensitive to various physical, chemical and biological agents as well as to genetic mutations. Any disturbance of the normal process may result in neuronal migration disorder. Such neuronal migration disorder is believed as major cause of both gross brain malformation and more special cerebral structural and functional abnormalities in experimental animals and in humans. An increasing number of instructive studies on experimental models and several genetic model systems of neuronal migration disorder have established the foundation of cortex formation and provided deeper insights into the genetic and molecular mechanisms underlying normal and abnormal neuronal migration.
D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000818:Animals; D015415:Biomarkers; D002352:Carrier Proteins / Q000032:analysis; D015816:Cell Adhesion Molecules, Neuronal / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D002465:Cell Movement; D002540:Cerebral Cortex / Q000002:abnormalities / Q000166:cytology* / Q000196:embryology / Q000254:growth & development; D016207:Cytokines; D016326:Extracellular Matrix Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008322:Mammals / Q000033:anatomy & histology / Q000196:embryology; D051379:Mice; D008818:Mice, Neurologic Mutants; D008831:Microcephaly / Q000235:genetics / Q000473:pathology; D008869:Microtubule-Associated Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D000078792:Midkine; D023421:Models, Animal; D009024:Morphogenesis; D009419:Nerve Tissue Proteins / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D009457:Neuroglia / Q000502:physiology; D009474:Neurons / Q000166:cytology*; D011247:Pregnancy; D051381:Rats; D000091042:Reelin Protein; D012697:Serine Endopeptidases; D013577:Syndrome; D013723:Teratogens / Q000633:toxicity; D014960:X Chromosome / Q000235:genetics; D015211:Zellweger Syndrome / Q000235:genetics / Q000473:pathology
D015415:Biomarkers; D002352:Carrier Proteins; D015816:Cell Adhesion Molecules, Neuronal; D016207:Cytokines; D016326:Extracellular Matrix Proteins; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins; D000091042:Reelin Protein; D013723:Teratogens; D000078792:Midkine; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; C084102:PAFAH1B1 protein, human; C513190:Pafah1b1 protein, mouse; D012697:Serine Endopeptidases