Chronically injured supraspinal neurons exhibit only modest axonal diebackin response to a cervical hemisection lesion

Authors
Citation
Jd. Houle et Y. Jin, Chronically injured supraspinal neurons exhibit only modest axonal diebackin response to a cervical hemisection lesion, EXP NEUROL, 169(1), 2001, pp. 208-217
Citations number
37
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL NEUROLOGY
ISSN journal
00144886 → ACNP
Volume
169
Issue
1
Year of publication
2001
Pages
208 - 217
Database
ISI
SICI code
0014-4886(200105)169:1<208:CISNEO>2.0.ZU;2-2
Abstract
This study examined the extent of axon retraction (dieback) exhibited by in jured brain stem neurons in a chronic spinal cord injury (SCI) condition. A dult female rats subjected to a cervical (C3) hemisection lesion were sacri ficed 1, 4, 8, or 14 weeks after injury and the spinal cord from C1 to the lesion cavity was removed. One week prior to sacrifice, a microinjection of biotinylated dextran amine (BDA, 0.5 mul) was made into the red nucleus, l ateral vestibular nucleus, or medullary reticular formation of each animal. Horizontal cryostat sections were processed with avidin-HRP to detect supr aspinal axons anterogradely labeled with BDA. Terminal end bulbs of axons w ere identified and their distance from the lesion site was measured by a co mputerized image analysis program. At all postinjury intervals, numerous ru brospinal, vestibulospinal, and reticulospinal tract axons were found immed iately adjacent to the lesion site and over 60% of all terminals were withi n 500 mum at 1 and 4 weeks. The mean axonal distance of 450-500 mum from th e lesion indicated that many injured axons had retracted farther than 500 m um from the lesion site; however, long-term maintenance of the mean axonal distance from the lesion at less than 500 mum indicated the absence of prog ressive dieback after SCI. While some modest changes occur in specific supr aspinal pathways following SCI, axonal retraction does not appear to be a c ontributing factor to the diminished regenerative effort by certain brain s tem neurons that has been observed at long postinjury intervals. (C) 2001 A cademic Press.