The effects of nerve section and of colchicine treatment on the density of mechanosensory nerve endings in salamander skin.

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Abstract
When one of the spinal nerves supplying the salamander [Amblystoma tigrinum] hind limb is cut or treated with colchicine, the fields of the remaining nerves enlarge in area; but nerve section produces Wallerian degeneration, the colchicine-treated nerves conducted action potentials normally and their peripheral fields remained unchanged in area. Since colchicine-treatment reduced neuronal transport, and nerve-section eliminated it, nerve sprouting may be regulated by factors normally conveyed to the endings by axoplasmic transport. The effects of colchicine on the thresholds and distribution of individual mechanosensory endings in the skin were investigated. If reduction of neuronal transport were enough to cause the threshold to be increased to the point of total unresponsiveness, then this could be a sign of an early stage of degeneration in those terminals. It might then be hypothesized that products of degeneration were providing a stimulus for adjacent nerves to sprout. Quantitative physiological studies of the effects of colchicine doses known to interfere with fast axoplasmic transport, indicated that in some experiments the terminal field of the treated nerve was invaded by sprouting fibers from neighboring axons, when its own endings were unchanged in number, distribution and sensory thresholds. In other experiments the colchicine-treated nerve endings showed an increase in threshold but their function was otherwise unchanged; a similar adjacent nerve sprouting occurred. In a final group, colchicine caused total unresponsiveness of some endings of the treated nerve. When a region of skin was partially denervated by nerve section, the physiological analysis indicated that the number of new mechanosensory endings which sprouted from the remaining axons exactly matched the number lost by nerve degeneration: the distribution of the endings was normal. It appears that sprouting ceased when the original density of mechanosensory endings in the skin was restored. The possibility that the drug induced sprouting as a consequence of a direct action on the skin is unlikely. With [3H]colchicine, the accumulation of label in the skin of the untreated limb, in which sprouting did not occur, equalled that of the opposite limb. Collateral sprouting of intact nerves apparently occurs when the supply of neuronally transported factors becomes inadequate to balance out the effects of a postulated target-tissue stimulus. Other examples of collateral nerve sprouting, such as that following adjacent denervation, were explained by this hypothesis.