Axotomy-induced increase in 2-deoxyglucose (2-DG) uptake by motor nuclei and neuronal chromatolytic changes were studied after subepineural injection of colchicine into the motor nerve. Hypoglossal nuclei of either cats or rats were axotomized bilaterally, while one of the nerves was injected with colchicine or saline proximal to the site of nerve transection and the other was left intact or injected with saline. Colchicine abolished or decreased the uptake of 2-DG by axotomized nuclei and delayed the onset of chromatolysis. The decrease in 2-DG uptake was observed in rat hypoglossal nuclei between 24 and 48 hr but not 5 days after drug treatment. In turn, a delay in the onset of chromatolysis was observed in cat hypoglossal nuclei at 14 days but not 30 days after treatment. Saline did not prevent chromatolysis nor the increased uptake of 2-DG. Colchicine injected intraneurally in intact preparations did not result in chromatolysis or in increased 2-DG uptake. Following colchicine injection, the drug remained localized near the site of injection and blocked retrograde axonal transport of horseradish peroxidase in the hypoglossal nerve. These findings suggest that the onset of chromatolysis and of the increase in 2-DG uptake after axotomy are partly dependent upon retrograde axonal transport.
SummaryThis study is concerned with the effect of colchicine on the structure of fibrillar constituents of neurons and on the transport of neuronal organelles. Colchicine was injected beneath the perineurium of the hypoglossal nerve. Close to the site of the injection, the 24 and 48 h experimental axons showed loss of microtubules, increased numbers of filaments and increased amounts of the microfilamentous material bridging the filaments. Evidence of organelle damming was found proximal to the site of the injection. Five days after the injection of colchicine the nerves appear to have recovered and resemble control nerves. It is speculated that the circumscribed increase in the amount of filaments and microfilaments may produce a 'gel barrier' that interrupts mechanically the movement of organelles.
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