title: Neurofilamentous hypertrophy of intramedullary axonal arbors in intact spinal motoneurons undergoing peripheral sprouting.
abstract: An incomplete motor nerve injury or a partial loss of motoneurons leads to a partial denervation of skeletal muscle. As part of a compensatory response, the remaining intact motoneurons undergo peripheral sprouting and increase their motor unit size. Our knowledge about the responses in the more proximal parts of these sprouting motoneurons is sparse, however. We investigated the effects of an incomplete transection of the medial gastrocnemius (MG) nerve in the adult cat on the morphology of the intramedullary axon and axon collateral systems of the remaining intact MG motoneurons. At twelve weeks following the partial transection of the MG nerve, intracellular recording and labeling techniques were used to deposit horseradish peroxidase into single intact MG motoneurons for detailed morphological studies. The light microscopic appearance and caliber of the intramedullary stem motor axons of the intact MG motoneurons were indistinguishable from controls. The number and size of the intramedullary motoraxon collateral systems were also unchanged. However, frequent and marked hypertrophy of the distal portions of the motoraxon collaterals was encountered. Electron microscopic studies of the hypertrophied collaterals demonstrated abnormal accumulations of disorganized neurofilaments arranged in bundles or whorls. The morphological changes were indistinguishable from the neurofilamentous hypertrophy that has previously been reported in Wallerian degeneration, in experimental and human motor neuron disease and in some regenerating axonal processes of spinal motoneurons. We conclude that, neurofilamentous hypertrophy of the intramedullary arbors of motor axons may also be part of a reactive and non-degenerative response in intact motoneurons undergoing compensatory peripheral sprouting.
authors.affiliation: Department of Neurology and Brain Research Institute, Neurologic Rehabilitation and Neural Repair Programs, University of California, Los Angeles, CA. 90095-1769, USA. LHavton@mednet.ucla.edu
authors.forename: L A
authors.initials: LA
authors.lastname: Havton
authors.forename: J O
authors.initials: JO
authors.lastname: Kellerth
mesh_terms: D000818:Animals; D001369:Axons / Q000648:ultrastructure*; D002415:Cats; D006735:Horseradish Peroxidase; D006984:Hypertrophy; D008854:Microscopy, Electron; D009046:Motor Neurons / Q000502:physiology* / Q000648:ultrastructure; D009121:Muscle Denervation; D018482:Muscle, Skeletal / Q000294:innervation; D009416:Nerve Regeneration; D014855:Wallerian Degeneration
chemical_list: D006735:Horseradish Peroxidase