![]() High-density and low-density lipoproteins, locally gathering needed material from an external source ( Vance et al. Similarly, experiments in sympathetic neurons demonstrate that the cell body is responsible for cholesterol synthesis,īut if synthesis is insufficient or is blocked pharmacologically, both the cell body and axons can take up cholesterol from 3, below) or in vivo show that at least some lipid synthesis can occur in axons ( Gould et al. Located throughout the axon, however, and experiments using radioactive lipid precursors added to axons but not to the cellīodies of neurons either in compartmented cultures (Fig. 1995a, b), although it is not clear how much this represents dependence on supply from the cell body or from the axon. Lipids? Blocking lipid synthesis interferes with axon growth ( Posse de Chaves et al. Reticulum (ER) and golgi complex are located, and shipped in vesicles down the axon for membrane insertion. Transmembrane and extracellular, as well as glycolipids are likely synthesized at the cell body, where the rough endoplasmic To elongate in culture ( Shaw and Bray 1977), but evidence for local production of membrane and cytoplasmic elements went lacking for decades. Where are the lipid and protein buildingīlocks made? It was known from classic experiments that axons cut off from the cell bodies of adult sensory neurons continue Rapid axon growth requires rapid manufacture and supply of cytoplasm and membrane. Production of the building blocks, both membrane and cytoplasmic Of axon growth and here I review recent answers and approaches to the above questions, and highlight their relevance during What are the intracellular molecular mechanisms by which they induce elongation? What controls the rate of axon growth? Howĭo CNS neurons know whether to extend axons or dendrites? Is the signaling of axon versus dendrite growth attributable toĭifferent extracellular signals, different neuronal states, or both? All of these questions bear critically on our understanding Steered through complicated pathways (for review, see Schmidt and Hall 1998 Mueller 1999), and even how neurons initiate new processes (for review, see Da Silva and Dotti 2002), but what mechanisms are involved in elongation itself? Are environmental signals needed to drive axon growth and, if so, Considerable attention in recent years has focused on understanding how growth cones are guided and ![]() The proper time is critical to understanding the development of our nervous system, yet the regulation of these processes Knowledge of how neurons extend axons and dendrites, elongate at a particular rate, and stop growing at The complex morphology of axons and dendrites puts neurons among the most intricate and beautifulĬells in the body. To wire up our nervous system properly, neurons must elongate their axons during development to reach their targets. System, the axon is the information superhighway, carrying all of the data we use to sense our environment and carry out behaviors. How do axons grow during development, and why do they fail to regrow when injured? In the complicated mesh of our nervous Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305, USA.
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