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The changes in neuronal number, cell body size and nuclear size have been followed for 12 weeks after postganglionic axotomy of the rat superior cervical ganglion. Axotomy was carried out at 6 days post partum and treatment with nerve growth factor (NGF) was from 6-21 days. During normal development there is a 30% decrease in the number of neurons in the superior cervical ganglion; axotomy increases the loss of cells resulting in a 90% decrease by 28 days post partum. The normal decrease is prevented and the enhanced loss of cells after axotomy is decreased by administration of NGF. Thus the increased number of cells observed after NGF administration appears to be due to the survival of cells that otherwise would have degenerated. NGF causes a rapid enlargement of both the cell bodies and the nucleus in the normal and axotomized ganglia. This increase in size rapidly reverses after cessation of treatment. These changes in cell size may account for the previously observed changes in cell profile number with NGF. There is a large increase in the number of non-neuronal cells during normal development and axotomy prevents this increase. NGF treatment results in a 6 fold increase in the number of non-neuronal cells and it is suggested that these are required to support the massive fibre outgrowth that occurs in NGF treated ganglia. It is concluded that these results are consistent with a physiological role for NGF as the trophic substance supporting adrenergic neurons making the appropriate contact with their target cell.

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Although brain-derived neurotrophic factor (BDNF) has been shown to promote peripheral myelination during development and remyelination after injury, the precise mechanisms mediating this effect remain unknown. Here, we determine that BDNF promotes myelination of nerve growth factor-dependent neurons, an effect dependent on neuronal expression of the p75 neurotrophin receptor, whereas BDNF inhibits myelination of BDNF-dependent neurons via the full-length TrkB receptor. Thus, BDNF exerts contrasting effects on Schwann cell myelination, depending on the complement of BDNF receptors that are expressed by different subpopulations of dorsal root ganglion neurons. These results demonstrate that BDNF exerts contrasting modulatory roles in peripheral nervous system myelination, and that its mechanism of action is acutely regulated and specifically targeted to neurons.