The axon determines whether or not it is myelinated by the Schwann cell. At maturity there is a positive correlation between sheath thickness and axon calibre. This correlation is initially very low or absent, but gradually strengthens during development. This increase could come about because the axon continuously controls Schwann cell myelinating activity, so that a given axon calibre is associated with a particular myelin sheath thickness, an interaction which would entail the Schwann cell continuously monitoring and responding to axon size. This seems unnecessarily complex. This theoretical study shows that the strong correlation between the 2 parameters within a given myelinated fibre population may come about in a much simpler way than outlined above. This is demonstrated by modelling the growth and myelination of a hypothetical population, utilising data from earlier studies on cervical ventral motoneuron axon development. The hypothesis tested shows that the only instructive interactions by the axon on the Schwann cell necessary for the strong correlation between the 2 parameters to emerge are for the initiation of myelination, its continuation and its termination. These could result from a single stimulus being switched on, persisting for a time and being switched off. Under this influence, the Schwann cell is assumed to proceed to form the myelin sheath at a constant rate which it itself inherently determines, in the absence of any quantitative influence exerted by the axon. This continues until the stimulus for myelination ceases to emanate from the axon. The validity of the hypothesis is demonstrated, because the resulting myelin-axon relationships correspond closely to those observed during development.

Pregnant female mice were divided on day 12 post coitum into a control and an experimental group. The experimental group was given a single intraperitoneal dose of 0.015 ml/g body weight of 25% solution of alcohol in distilled water while the control group was exposed to a similar weight related dose of normal saline. The optic nerves were isolated from the offspring of both control and experimental groups at wk 2, 3 and 5 (i.e. during the juvenile period of postnatal development) and analysed by light and electron microscopy. Although in both groups the optic nerve grew in size rapidly during the period studied, the rate of growth in the experimental groups lagged behind that of the controls. The difference was initially significant but tailed off, so that by wk 5 it was no longer significant. The time of initial onset and progression of myelinogenesis in the optic nerve of alcohol exposed mice also lagged behind that of controls. In both groups the size distribution of the myelinated nerve fibres in the optic nerve was unimodal with a positive skewing for all ages. The spectrum of size distribution of the nerve fibres was, however, broader in controls than in the corresponding experimental groups. With increasing age the proportion of small and medium size fibres was greater in the experimental group than in the controls, while for the large diameter fibres the reverse was observed. It is suggested that this study may shed light on the teratogenic effect of ‘binge’ drinking during pregnancy and that it is the critical period when exposure occurs that is more important than the duration of administration.