Summary

1. Pleiotropy is a condition in which a single gene contributes to many different traits, as when a failure of cell migration causes the many disparate symptoms of Kallmann syndrome. See Figure 3.1
2. In the neural tube, mitosis occurs when the cell nuclei are near the ventricular surface. As the tube thickens, cells may span the width of the tube, but the nuclei will still shift to the ventricular surface during mitosis. See Figure 3.2
3. Symmetrical divisions provide more neuroblasts, including some cells that will later serve as radial glial cells. Asymmetric divisions produce one postmitotic daughter cell that joins the outermost marginal zone or, later, the cortical plate to differentiate into a neuron (neurogenesis) or glia (gliogenesis). See Figures 3.3 and 3.4
4. Studies using cell lineage markers in chicks and mice show that the progeny of a single neuroblast may take on many different fates, indicating little or no role of mitotic lineage in cell differentiation. See Figure 3.5
5. In the cerebral cortex, some neuroblasts detach from the ventricular zone to form the subventricular zone (SVZ), continuing to divide to produce neurons and glia. See Figures 3.6 and 3.7
6. A few of the earliest-generated neurons settle in the sparsely populated layer I, but thereafter each cohort of neurons migrates past their predecessors, settling in an “inside-out” order, with innermost layer VI containing the oldest neurons and layer II the youngest. See Figures 3.10–3.12
7. Some neurons arise from one of three ganglionic eminences and migrate tangentially across radial glia rather than simply out a single glial fiber. In humans, an arc of new neurons is still migrating into the frontal cortex in the first few months of life. See Figures 3.13 and 3.14
8. Neurogenesis extends into adulthood in three regions: the olfactory epithelium producing replacement olfactory sensory neurons, the SVZ of the lateral ventricles that supply the rostral migratory stream of olfactory bulb interneurons, and the subgranular zone of the dentate gyrus in the hippocampal formation. See Figures 3.15 and 3.16
9. Although it is not universally accepted, there is considerable evidence that a few new neurons are also added to the adult neocortex and that experience affects the production or survival of these new neurons. See Figure 3.17
10. Neural crest cells contribute to the pharyngeal arches that make up cranial nerve ganglia, and in the spinal regions they will migrate out four major pathways to form dorsal root ganglia, autonomic ganglia, the adrenal medulla, and melanocytes. See Figures 3.18–3.20
11. Crest cells regulate expression of cell adhesion molecules and secrete proteases to start their migration, then follow paths of cell adhesion molecules to reach their destination. They display a strong preference to migrate along pathways rich in the glycoprotein fibronectin. See Figure 3.21
12. Migrating crest cells are also herded into one stream per spinal segment by avoidance of the ephrins expressed in the posterior half of each somite. See Figure 3.22
13. Cerebellar Purkinje cells arise from the ventricular layer to form a single layer. Granule cells arise from the rhombic lip to migrate over the dorsal surface of the cerebellar cortex, continue dividing in that external granule layer, and then migrate down along Bergmann glia fibers past the Purkinje cells to form the internal granule layer. See Figures 3.24–3.26
14. Migrating granule cells are also guided by adhesive signals. The weaver mutation makes the cells incapable of grasping glia in order to migrate properly. In reeler mutants, the lack of reelin secretion from the external granule layer means Purkinje cells don’t align in a single layer, severely disrupting the subsequent migration of cells to the internal granule cell layer. See Figures 3.28–3.30
15. Cells from the olfactory placode provide primary olfactory sensory neurons that send axons through the cribriform plate to synapse in the olfactory bulb, as well as cells that become olfactory ensheathing glia along those axons, plus cells that migrate along those axons to enter the hypothalamus and become GnRH neurons. Kallmann syndrome results when the primary olfactory sensory neurons don’t form, depriving the person of a sense of smell and denying presumptive GnRH neurons a pathway into the brain. See Figure 3.31