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Journal of Neuroscience, Vol 15, 2756-2767, Copyright © 1995 by Society for Neuroscience
Increased collateral sprouting of primary afferents in the myelin-free spinal cord
G Schwegler, ME Schwab and JP Kapfhammer
Brain Research Institute, University of Zurich, Switzerland.
After partial lesions, uninjured nerve fibers have been shown to sprout and
expand their connections within the CNS of adult mammals. The extent of
this anatomical plasticity in adults is rather limited in comparison to
embryonic or neonatal animals. Factors that might limit sprouting of nerve
fibers and suppress anatomical plasticity in the CNS include
myelin-associated neurite growth inhibitory molecules present in the CNS of
adult mammals. To examine further the role of these neurite growth
inhibitors, we have studied the ability of primary afferent fibers to
sprout in the absence of myelin within a partially deafferented spinal
cord. Myelination was suppressed in the lower thoracic and lumbar spinal
cord of rats using neonatal x-irradiation. Dorsal roots of lumbar segments
L2-L4 were cut in myelin-free and normal spinal cords of 8- or 15-d-old
rats. Sprouting of primary afferents was measured after 20 d using thiamine
monophosphatase (TMP) histochemistry. TMP is a specific marker enzyme for
small-diameter primary afferents that terminate in the substantia
gelatinosa (lamina II) of the spinal cord. When compared to the control
groups, collateral sprouting of TMP-positive afferents was significantly
enhanced in the myelin-free spinal cords: in animals deafferented at
postnatal day P8, the average volume occupied by sprouting fibers in the
upper dorsal horn was 0.103 mm3 +/- 0.008 (mean +/- SEM) in myelin-free
spinal cords and 0.044 mm3 +/- 0.011 in control spinal cords. In spinal
cords deafferented at P15, this difference was even larger, with 0.106 mm3
+/- 0.010 in the absence of myelin and 0.031 mm3 +/- 0.010 in controls. Our
results indicate that myelin and its associated neurite growth inhibitors
restrict collateral sprouting. These data provide further evidence that CNS
myelin and its associated neurite growth inhibitors are involved in the
regulation of anatomical plasticity in the normal CNS.
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