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The Changes in Human Spinal Sympathetic Preganglionic Neurons After Spinal Cord Injury

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The Changes in Human Spinal Sympathetic Preganglionic Neurons After Spinal Cord Injury Spinal Cord (1999) 37, 6±13 ã 1999 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/99 $12.00 http://www.stockton-press.co.uk/sc The changes in human spinal sympathetic preganglionic neurons after spinal cord injury AV Krassioukov1, RP Bunge2, WR Pucket2 and MA Bygrave1 1The Neurodegeneration Research Group, The JP Robarts Research Institute, The Department of Physiology of the University of Western Ontario, 100 Perth Drive, PO Box 5015, London, Ontario, Canada; 2The Miami Project to Cure Paralysis, University of Miami School of Medicine, Miami, Florida 33136, USA We have applied conventional histochemical, immunocytochemical and morphometric techniques to study the changes within the human spinal sympathetic preganglionic neurons (SPNs) after spinal cord injury. SPNs are localized within the intermediolateral nucleus (IML) of the lateral horn at the thoraco-lumbar level of the spinal cord and are the major contributors to central cardiovascular control. SPNs in dierent thoracic segments in the normal spinal cord were similar in soma size. SPNs in the IML were also identi®ed using immunoreactivity to choline acetyltransferase. Soma area of SPNs was 400.7+15 mm2 and 409.9+22 mm2 at the upper thoracic (T3) and middle thoracic (T7) segments, respectively. In the spinal cord obtained from a person who survived for 2 weeks following a spinal cord injury at T5, we found a signi®cant decrease in soma area of the SPNs in the segments below the site of injury: soma area of SPNs at T8 was 272.9+11 mm2. At T1 the soma area was 418+19 mm2. In the spinal cord obtained from a person who survived 23 years after cord injury at T3, the soma area of SPNs above (T1) and below (T7) the site of injury was similar (416.2+19 and 425.0+20 mm2 respectively). The ®ndings demonstrate that the SPNs in spinal segments caudal to the level of the lesion undergo a signi®cant decrease of their size 2 weeks after spinal cord injury resulting in complete transection of the spinal cord. The impaired cardiovascular control after spinal cord injury may be accounted for, in part, by the described changes of the SPNs. The SPNs in spinal segments caudal to the injury were of normal size in the case studied 23 years after the injury, suggesting that the atrophy observed at 2 weeks is transient. More studies are necessary to establish the precise time course of these morphological changes in the spinal preganglionic neurons. Keywords: atrophy; cardiovascular control; spinal cord injury; morphometry Introduction Cardiovascular control in the human is signi®cantly matter below the spinal cord injury could play a impaired after spinal cord injury.1±3 Clinical observa- crucial role in determining long term neurological tions provide much of our current understanding of the outcome.11 ± 13 characteristics of this disabling condition;4±6 however, This study used a novel approach to study changes little is known about the morphological changes that in spinal sympathetic preganglionic neurons (SPNs) occur within the spinal cord structures which control after spinal cord injury in order to understand the the cardiovascular system. A substantial portion of the mechanisms underlying the impaired cardiovascular current literature on spinal cord pathology is focused control. In this study we examined the eect of partial on characterizing the changes at the site of injury. Such deaerentation (loss of supraspinal descending path- work often describes the extent of demyelination or ways) of spinal cord neurons by a complete spinal cavitation within the human spinal cord, or de®nes injury. As the eerent component of the central complete or incomplete injuries of the spinal cord.7±11 nervous system (CNS), SPNs send tonic signals to After spinal cord injury, preservation of descending dierent target organs such as blood vessels, the heart pathways through the area of cord injury or the and the adrenal medulla, therefore, SPNs are crucial maintenance of neuronal populations in the gray for central cardiovascular control.14±16 Previous research in animal models demonstrated that follow- ing spinal cord transection, SPNs show signs of Correspondence: Dr A Krassioukov, The John P. Robarts Research atrophy in the acute stage of spinal injury. However, Institute, 100 Perth Drive, P.O. Box 5015, London, Ontario with time in the chronic stage SPNs regain their N6A 5K8, Canada 17 RP Bunge, deceased normal morphology. These morphological changes Human preganglionic neurons after spinal cord injury AV Krassioukov et al 7 within the SPNs may occur as a result of partial made in donkey (1 : 400 dilution, Biocan Scienti®c, deaerentation, because of a loss of descending Canada) and rhodamine lissamine conjudated to projections from medullary neurons. A portion of streptavidin antibody (1 : 150 dilution Biocan Scien- the descending medullary input to SPNs is thought to ti®c, Canada) were used for staining.25 Immunofluor- synapse directly.18 Previously, neurons within the escent neurons were detected using a Leitz microscope lateral horn of the human cord were studied only in equipped with an epi¯uorescence system containing cases with multiple system atrophy and autonomic N2 ®lter. failure.19 ± 21 In our study, we investigated the changes First, the sections were examined under a bright in humans SPNs following spinal cord injury and ®eld microscope for the gross anatomy. The presence compared this with our previous animal ®ndings.17 of major artifacts within examined segments was The SPNs within the human spinal cords were determined. Then examination was focused only on identi®ed. The soma area and diameter of SPNs were the lateral horns of the spinal cord. This is a clearly analyzed in one case with intact spinal cord and in two identi®ed area of the spinal cord (Figures 1A, 2A and cases after spinal cord injury. The cases with human C). The location and morphology of SPNs were spinal cord injury were chosen on the basis of data analyzed using a Leitz microscope with the Micro- from previous animal experiments.17 Therefore, the computer Imaging Device imaging system (MCID, St. cases of acute and chronic spinal injury were selected Catharines, Ontario). The somas were outlined and and anatomical completeness was con®rmed for assessed for area size, median and maximum diameters comparison of SPNs. SPNs were compared in upper using MCID software. The majority of measured cells and middle thoracic (T) segments in the control case were elongated, not circular. In elongated targets the and above and below the site of injury in cord-injured median diameter is a measure of width, while the cases. maximum diameter is a measure of length.26 There- fore, both diameters were chosen for a better Methods representation of spatial dimensions of the measured cells. Only preganglionic neurons within the inter- Two spinal cords from persons who had suered spinal mediolateral nucleus (IML) of the spinal cord, as a cord injury prior to death were selected from the bank clearly identi®ed area of the spinal cord, were analyzed of autopsy materials at the Miami Project to Cure (Figure 1). Moreover, this area of the cord contained Paralysis of the University of Miami School of cholinergic neurons identi®ed by the presence of Medicine. One specimen of spinal cord from a person ChAT. In each segment at least 20 SPNs were without spinal injury was provided by the Department selected and soma area, median and maximum of Pathology from the London Health Sciences Centre, diameters were measured and compared in upper and University Campus, The University of Western middle thoracic segments of the spinal cords. In the Ontario. two cases with spinal cord injury we were able to Spinal cords were removed within 24 h of death in compare the SPNs above and below the site of spinal all three cases. The cords were placed immediately in injury. The neurons below the injury represent neurons 10% buered formalin for a period of 2 weeks, and which lost descending input from supraspinal struc- then stored in phosphate buer (0.1 M,pH7.2)at48C. tures. To eliminate bias of the observer, measurements In the cases with spinal cord injury, the site of injury were made without the knowledge of the segment and was examined and the completeness of injury was case number. The age and sex factor was eliminated by determined. The level of damage was determined by choosing the specimens from men of the same age. physical examination of the cord and root identifica- tion. The severity of the injury (complete/incomplete) was determined from histological analysis of the site of Statistical analysis injury. The quantitative cell analysis was used cautiously in Alternative axial sections of the spinal cords were our study. To determine statistical morphological prepared and examined in all three cases. Three sets of dierences in the SPNs at dierent levels of the 30 ± 40 sections were prepared from each segment of human spinal cord and between the cases, a one-way the spinal cords in each case. One set of sections was analysis of variance with repeated measures was used. stained for general histology (haematoxylin-eosin). Tukey's test was used for comparison of mean values.27 The second set of sections was stained for neurons All data in the paper were presented as mean+SEM. and their processes using a silver staining technique Dierences were considered signi®cant when P50.05. (Bielchowsky).22 Finally, the third set of sections was processed immunocytochemically for choline acetyl- transferase (ChAT). Antigen retrieval incorporating Results high-temperature microwave heating of formalin-®xed, paran-embedded tissue sections before immunostain- Case 1 (Case with normal spinal cord) ing was used in this case.23,24 Antibodies to ChAT This 43-year-old male had died from myocardial made in goat (1/1000 dilution; Chemicone, USA) were infarction.
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