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It might be suggested that autonomic motor neurons seem to become affected by the same pathologic process that kills motor neurons.
The process seems likely to be similar to that affecting motor neurons but is less advanced at the time of death.
These observations suggest that galanin and CGRP participate in the process of synaptic transmission at the neuromuscular junction of cranial motor neurons.
This suggests that the cerebellum can exert and influence not only on the cortical interneurons but also on neurons directly concerned with motor function.
They also provide further evidence for activity-dependent maturation of motor neurons.
The prominent degeneration of motor neurons, however, must also have played a role in the clinical picture.
We found that many degenerating spinal motor neurons were not infected directly with NSV, suggesting that bystander cell death occurs.
These findings imply varying resistance to the disease in different pools of motor neurons.
We hypothesize that both phenomena are not only crucial for the normal functioning of motor neurons, but that they could also be interconnected.

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