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Acetylcholinesterase (AChE) activity and its fast axonal transport were studied in rabbit sciatic nerves with a double ligature system during the recovery phase of experimental allergic neuritis (EAN), 6-9 days after the maximal symptoms, in order to obtain biochemical evidence of possible axonal damage in this primary demyelinating disease. The stationary AChE activity was significantly decreased, but the amount of the fast transported enzyme activity remained at the level of the controls. The velocity of the orthograde transport of AChE was slowed by about 15%, but this decrease was not statistically significant. Our results lend further support for the suggested neuronal damage in EAN, which can provide an explanation to the finding that the clinical symptoms in demyelinating diseases of the peripheral nervous system do not always correlate with the state of myelin.