By C. Bell
This quantity presents an updated survey of present considering about the activities of chemical components within the rules of neuronal behaviour below general and pathological stipulations. The booklet is split into 4 sections, facing chemical elements concerned with the formation of axon pathways, elements concerned with neuronal survival and specialization in the course of general improvement, elements fascinated by general upkeep and service of grownup neurons and, ultimately, components which have been implicated as mediators of degenerative adjustments in neurological and neuropsychiatric issues.
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Additional resources for Chemical Factors in Neural Growth, Degeneration and Repair
Whitington 29 Fig. 18. Axon growth from neurons pioneering longitudinal axon pathways in the CNS of wild-type and fasciclin II null mutant Drosophila embryos. (A) Schematic diagram of a dorsal view of pioneering neurons in a wild-type embryo at embryonic stage 13. The posteriorly projecting MPl and dMP2 axons fasciculate with the anteriorly projecting axons from pCC and vMP2 in regions 1 and 2. All of these axons adhere to the ventral surface of the longitudinal glial cell LGX. (B) Fasciclin II null mutant at the same stage as (A).
Bray and Chapman, 1985). This model was widely accepted and heavily influenced interpretation of the pioneering observations of axon growth in insect embryos. Recent observations in a variety of animals, but notably in several invertebrates, have begun to cast doubt on this model as a sufficient explanation for growth cone turning. The mollusc Aplysia has been a favoured organism for in vitro studies of growth cone structure and function because several identified neurons of this species, such as the buccal ganglion neurons Bl and B2, form large, expanded growth cones in culture.
1995), although defects are seen in late 18 Axon guidance factors in invertebrate embryos. On the other hand, Hidalgo et al. (1995) report that ricin induced ablation of the longitudinal glial cells leads to a failure of formation of longitudinal connectives in 71% of embryos. Menne and Klambt (1994) used a temperaturesensitive allele of the neurogenic gene Notch to delete midline glial cells in Drosophila and found a correlation between absence of these cells and MP133a lOOum Fig, 13. The effect of ablation of the muscle pioneer cell MP133a on axon outgrowth from the Df motoneuron in the grasshopper embryo.