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Neuroscience. 1992 Oct;50(4):975-86.

The use of a neurotoxic lectin, volkensin, to induce loss of identified motoneuron pools.

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Department of Anatomy and Developmental Biology, University College of London, U.K.


In this study we investigated degeneration of defined motor pools in the adult rat spinal cord and the associated changes in spinal cord in dorsal root ganglia and peripheral nerve. Degeneration of motoneurons was induced by the neurotoxic lectin, volkensin. This substance is taken up by the axons and retrogradely transported to the cell body, where it inhibits proteosynthesis and kills the neuron. Accordingly, in adult Wistar rats the peroneal or the sciatic nerve was injected with 5.0 ng volkensin, and the effect of this single injection was investigated at different intervals after the operation. Retrograde labelling by horseradish peroxidase was used to reveal the extent of cell death and glial repair was studied by immunostaining with different glial cell markers. Degenerating cells were observed in the ventral horn of the lumbar spinal cord and L4 and L5 dorsal root ganglia as early as four days after volkensin treatment and by two weeks no retrogradely labelled motoneurons could be found in the treated peroneal pool. These changes were accompanied by severe muscle weight loss. Examination of the ventral horn of the spinal cord on the treated side revealed many hypertrophic astrocytes and reactive microglial cells expressing an increased level of complement receptor type 3 immunoreactivity. In the volkensin-injected peripheral nerve, distinct signs of Wallerian-like degeneration could be observed. Schwann cells identified by immunostaining to S-100 protein appeared to be preserved. Interestingly, at later stages after volkensin injection (four to eight weeks), some retrogradely labelled motoneurons were seen in the peroneal pool; their number occasionally reached 18.4% of the control pool. The dorsal root ganglia showed extensive loss of neurons and numerous abnormal neurons were found throughout the period of the study. These findings suggest that some motoneurons are able to recover from exposure to volkensin and temporary arrest of proteosynthesis. Despite this, volkensin-induced selective motoneuron death in the adult rat can be a useful experimental model for degenerative motoneuron disease.

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