Nodal and terminal sprouting by regenerating nerve in vitamin E-deficient rats.
The increased number of poly-innervated cells in normal and reinnervated extensor digitorum longus (edl) muscle of vitamin E-deficient rats suggests enhanced sprouting by motor neurons in conditions of decreased protection against lipid peroxidation. End-plates and terminal axons were observed by a combined technique that shows both end-plate acetylcholinesterase area and axons. Quantitative observations of nodal and terminal sprouting in normally innervated and reinnervated edl muscles of vitamin E-deficient rats were carried out. Branch points of nerve terminal within end-plates were also observed. Three main results were obtained. First, a notable increase of both terminal and nodal sprouting was found in reinnervated muscles of normal and vitamin E-deficient rats; moreover, a relative increase in the number of nodal sprouts occurs in the long run. Second, in muscles of uninjured, vitamin E-deficient rats, nodal and terminal sprouting and branching within end-plate was greater than in controls. Third, nodal sprouting by regenerating axons was more affected by vitamin E-deficiency than terminal sprouting and branching within end-plates.
Cuppini
R
R
Institute of Morphological Sciences, University of Urbino, Italy.
Cecchini
T
T
Ciaroni
S
S
Ambrogini
P
P
Del Grande
P
P
D000110:Acetylcholinesterase / Q000032:analysis; D000818:Animals; D001369:Axons / Q000648:ultrastructure; D015227:Lipid Peroxidation; D008297:Male; D009045:Motor Endplate / Q000201:enzymology / Q000648:ultrastructure; D009046:Motor Neurons / Q000502:physiology*; D009409:Nerve Crush; D009416:Nerve Regeneration; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000293:injuries / Q000502:physiology*; D014811:Vitamin E Deficiency / Q000503:physiopathology*
D000110:Acetylcholinesterase