Close axonal injury of rubrospinal neurons induced transient perineuronal astrocytic and microglial reaction that coincided with their massive degeneration.

To learn more about the pathophysiology of axonal injury and the significance of axon collaterals on the survival of axotomized cord-projection central neurons, we studied the survival rate, surrounding astrocytic and microglial reactions, and bouton coverage on rat rubrospinal cell bodies following their axonal lesion at the brain stem and upper cervical level. The brain stem lesion disconnected most rubrospinal neurons from all their targets, while the upper cervical lesion spared their supraspinal collaterals. Much higher cell loss accompanied by robust astrocytic and microglial reaction was found following brain stem than upper cervical lesion starting 4 days postaxotomy. The reaction of astrocytes had subsided while microglial reaction remained relatively robust by 10 weeks postaxotomy when the cell loss had slowed down. Ultrastructural observation revealed that reactive astrocytes covered 40%, an increase from the 20% of control, of brain stem-axotomized rubrospinal cell body surface at 4 days and 2 weeks and returned to normal levels by 10 weeks postlesion. An increase of apposition by axons and dendrites and a moderate decrease of round and flattened vesicle-containing bouton contacts at 4 days and 2 weeks and returning to normal levels at 10 weeks postaxotomy accompanied this. It appears that although axotomy induced robust astrocytic reaction around cord-projection central neurons, this, unlike their periphery-projection counterparts, failed to effectively strip their somatic synapses. In effect, this might in part determine neuronal fate following axonal injury.