Enhancement of sensitivity to acrylamide after nerve ligature.

Abstract

Acrylamide given to rats after damage to the posterior tibial nerve by a tight ligature causes retrograde degeneration of axons. The number of fibres affected and the extent of degeneration towards the cell body are dose dependent. The effect is the same whether the acrylamide is given immediately after ligature or one week later. The degeneration is delayed several days after giving acrylamide. Before axonal disintegration occurs, focal accumulations of SER, vesicle and multivesicular bodies are seen beneath the axon membrane. Associated with these changes larger vacuoles occur, either in the axon or external to it. It is suggested that these early changes are a response by the axon and perikaryon to the local metabolic damage caused by the toxic chemical. Somewhat similar changes also occur in early predegenerative INH intoxication, and before the axon degeneration in O-P neurotoxicity.