Literature DB >> 10025688

The changes in human spinal sympathetic preganglionic neurons after spinal cord injury.

A V Krassioukov1, R P Bunge, W R Pucket, M A Bygrave.   

Abstract

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 different thoracic segments in the normal spinal cord were similar in soma size. SPNs in the IML were also identified using immunoreactivity to choline acetyltransferase. Soma area of SPNs was 400.7+15 microm2 and 409.9+/-22 microm2 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 significant 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 microm2. At T1 the soma area was 418+/-19 microm2. 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 microm2 respectively). The findings demonstrate that the SPNs in spinal segments caudal to the level of the lesion undergo a significant 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.

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Year:  1999        PMID: 10025688     DOI: 10.1038/sj.sc.3100718

Source DB:  PubMed          Journal:  Spinal Cord        ISSN: 1362-4393            Impact factor:   2.772


  18 in total

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Review 3.  Autonomic dysreflexia after spinal cord injury: Systemic pathophysiology and methods of management.

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Journal:  Auton Neurosci       Date:  2017-05-08       Impact factor: 3.145

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5.  Chronic Spinal Cord Injury Reduces Gastrin-Releasing Peptide in the Spinal Ejaculation Generator in Male Rats.

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Journal:  J Neurotrauma       Date:  2019-07-10       Impact factor: 5.269

Review 6.  Cold pressor test in spinal cord injury-revisited.

Authors:  Michèle Hubli; Doris Bolt; Andrei V Krassioukov
Journal:  Spinal Cord       Date:  2017-12-20       Impact factor: 2.772

7.  Serum leptin levels following acute experimental spinal cord injury.

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8.  Impact of tetraplegia vs. paraplegia on venoarteriolar, myogenic and maximal cutaneous vasodilation responses of the microvasculature: Implications for cardiovascular disease.

Authors:  Michelle Trbovich; Yubo Wu; Wouter Koek; Joan Zhao; Dean Kellogg
Journal:  J Spinal Cord Med       Date:  2020-06-04       Impact factor: 1.985

9.  Associations between left ventricular structure and function with cardiorespiratory fitness and body composition in individuals with cervical and upper thoracic spinal cord injury.

Authors:  Abdullah A Alrashidi; Shane J T Balthazaar; Katharine D Currie; Tom E Nightingale; Andrei V Krassioukov
Journal:  Spinal Cord       Date:  2020-12-07       Impact factor: 2.772

10.  Plasticity of TRPV1-Expressing Sensory Neurons Mediating Autonomic Dysreflexia Following Spinal Cord Injury.

Authors:  Leanne M Ramer; A Peter van Stolk; Jessica A Inskip; Matt S Ramer; Andrei V Krassioukov
Journal:  Front Physiol       Date:  2012-07-09       Impact factor: 4.566

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