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Regenerative axonal sprouting in the cat trochlear nerve
Author(s) -
Iannuzzelli Pasquale G.,
Murray Marion,
Murphy E. Hazel
Publication year - 1995
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.903540206
Subject(s) - biology , sprouting , neuroscience , anatomy , trochlear nerve , regeneration (biology) , microbiology and biotechnology , pathology , medicine , alternative medicine , palsy , botany
Following peripheral trochlear nerve axotomy in the cat, the normal number of myelinated axons is restored despite significant motor neuron death, suggesting regulation of the number of myelinated axons in the regenerated nerve. In this study we used light and electron microscopy to examine the production and maintenance of axonal sprouts at different locations in the nerve and at different postoperative intervals. Despite proliferative sprouting and an overproduction of nonmyelinated axons in the regenerating trochlear nerve, the number of myelinated axons was strictly regulated. Only ∼1,000 regenerated axons were eventually remyelinated, but many nonmyelinated axons were still present 6–8 months postaxotomy. Regenerated axons were remyelinated in a proximal‐to‐distal direction between 3 and 4 weeks postaxotomy. We also examined the maturation of regenerated myelinated axons by measuring axon diameter and myelin index (an expression of myelin thickness). Mean myelinated axon diameter remained significantly below normal in long‐term regenerated nerves. Mean myelin index was not different from normal at 4 weeks postaxotomy but was significantly decreased at long postoperative intervals, reflecting a slightly thicker myelin sheath relative to the axon diameter. This relative increase in mean myehn thickness could serve to restore normal conduction velocity despite the decrease in mean axon diameter. We suggest that the regulation of the number of myelinated axons at the normal number despite cell death and the increase in mean myelin thickness may both be compensatory mechanisms that function to restore preoperative conditions and maximize functional recovery. © 1995 Wiley‐Liss, Inc.