This thesis is in two major sections: (1) Segmental sensory innervation: During the segmental, sensory innervation of the periphery, neurones situated in the dorsal root ganglia grow out axons at different rates. These vary with segmental level of the ganglia. The most rapid rates of axonal advancement are seen from those ganglia which innervate limb as opposed to non-limb ganglia. How are these differential axonal growth rates controlled? This problem has been addressed using cell culture techniques. No evidence for a segmentally regulated, intrinsic growth mechanism has been found. Further some common constituents of the peripheral fiels of these neurones were also, on the whole, ineffective in regulating neurite growth rates in culture. I conclude from this that some, as yet, unidentified factor in the periphery is reponsible for the enhanced growth rate of axons into limb tissue. A number of differences in the neurite growth patterns of neurones isolated from embryos at different stages of development were noted. This suggests that neurite growth is regulated developmentally if not segmentally. Neurite lengths from cultured neurones were found to benon-normally distributed. They showed a positively skewed, multimodal form. This was not explained by differences in neurite length, branch pattern or the stage of development of the neurones. In the light of this, a quantal hypothesis of neurite growth is proposed, and modelled using Poisson statistics as a theoretical basis. (2) Neuronal toxicity of cytosine-B-D-Arabinofuranoside: Cytosine-B-D-Arabinofuranoside (AraC) is a commonly used anti-mitotic agent in neural cultures. In this study it is also shown to be toxic to cultured neurones and to inhibit neurite growth. This toxicity is dose dependent and inhibited in the presence of 2'DeoxyCytidine (a metabolic precursor of AraC). A relationship between high metabolic demand (neurite growth) and AraC toxicity is discussed in the light of other experimental work.