scholarly journals Upregulation of EphA Receptor Expression in the Injured Adult Rat Spinal Cord

2002 ◽  
Vol 11 (3) ◽  
pp. 229-239 ◽  
Author(s):  
Christopher A. Willson ◽  
Margarita Irizarry-Ramírez ◽  
Hope E. Gaskins ◽  
Lillian Cruz-Orengo ◽  
Johnny D. Figueroa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Gray Matter ◽  
Receptor Expression ◽  
Axonal Guidance ◽  
Receptor Subtypes ◽  
Rat Spinal Cord ◽  
Functional Connections ◽  
Cord Injury ◽  
Epha Receptor

After spinal cord injury (SCI), the inability of supraspinal neurons to regenerate or reform functional connections is likely due to proteins in the surrounding microenvironment restricting regeneration. EphAs are a family of receptor tyrosine kinases that are involved in axonal guidance during development. These receptors and their ligands, the Ephrins, act via repulsive mechanisms to guide growing axons towards their appropriate targets and allow for the correct developmental connections to be made. In the present study, we investigated whether EphA receptor expression changed after a thoracic contusion SCI. Our results indicate that several EphA molecules are upregulated after SCI. Using semiquantitative RT-PCR to investigate mRNA expression after SCI, we found that EphA3, A4, and A7 mRNAs were upregulated. EphA3, A4, A6, and A8 receptor immunoreactivity increased in the ventrolateral white matter (VWM) at the injury epicenter. EphA7 had the highest level of immunoreactivity in both control and injured rat spinal cord. EphA receptor expression in the white matter originated from glial cells as coexpression in both astrocytes and oligodendrocytes was observed. In contrast, gray matter expression was localized to neurons of the ventral gray matter (motor neurons) and dorsal horn. After SCI, specific EphA receptor subtypes are upregulated and these increases may create an environment that is unfavorable for neurite outgrowth and functional regeneration.

Presence and significance of CD-95 (Fas/APO1) expression after spinal cord injury

2001 ◽  
Vol 94 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Mercedes Zurita ◽  
Jesús Vaquero ◽  
Isabel Zurita
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Gray Matter ◽  
Spinal Cord Tissue ◽  
Injured Spinal Cord ◽  
Content Type ◽  
Cord Injury ◽  
Positive Immunostaining ◽  
Fine Print

Object. A glycoprotein, CD95 (Fas/APO1) is widely considered to be implicated in the development of apoptosis in a number of tissues. Based on the hypothesis that apoptosis is related to cell death after spinal cord injury (SCI), the authors studied the presence and distribution of CD95 (Fas/APO1)-positive cells in injured spinal cord tissue for the purpose of determining the significance of this protein during the early phases of SCI. Methods. The presence and distribution of cells showing positive immunostaining for CD95 (Fas/APO1) were studied 1, 4, 8, 24, 48, and 72 hours and 1, 2, and 4 weeks after induction of experimental SCI in rats. Studies were conducted using a monoclonal antibody to the CD95 (Fas/APO1) protein. Positivity for CD95 (Fas/APO1) was observed in apoptotic cells, mainly in the gray matter, 1 hour after trauma, and the number of immunostained cells increased for the first 8 hours, at which time the protein was expressed in both gray and white matter. From 24 to 72 hours postinjury, the number of immunostained cells decreased in the gray matter, but increased in the white matter. From then on, there were fewer CD95 (Fas/APO1)-positive cells, but some cells in the white matter still exhibited positive immunostaining 1 and 2 weeks after injury. At 4 weeks, there remained no CD95 (Fas/APO1)-positive cells in injured spinal cord. Conclusions. These findings indicate that CD95 (Fas/APO1) is expressed after SCI, suggesting a role for this protein in the development of apoptosis after trauma and the possibility of a new therapeutic approach to SCI based on blocking the CD95 (Fas/APO1) system.

Effect of aminophylline and isoproterenol on spinal cord blood flow after impact injury

1980 ◽  
Vol 53 (3) ◽  
pp. 385-390 ◽  
Author(s):  
Diana Dow-Edwards ◽  
Vincent DeCrescito ◽  
John J. Tomasula ◽  
Eugene S. Flamm
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Cord Blood ◽  
Gray Matter ◽  
Adenosine Monophosphate ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Cord Injury ◽  
Matter Flow

✓ A study of the effects of spinal cord injury upon spinal cord blood flow was carried out in cats. A 400 gm-cm impact produced an overall reduction in spinal cord blood flow of 24% in the white matter and 30% in the gray matter, as determined by 14C-antipyrine autoradiography. At the level of the injury, white-matter flow was 8.1 ml/100 gm/min, a reduction of 49%, and in the gray matter, 12.5 ml/100 gm/min, a reduction of 76%. Treatment with aminophylline and isoproterenol improved the overall blood flow in the spinal cord. At the level of the injury, white-matter flow after this treatment was no longer significantly different from control values. The gray-matter flow remained decreased to 26.2 ml/100 gm/min, a reduction of only 47%. It is proposed that aminophylline and isoproterenol may increase cyclic adenosine monophosphate (AMP) and prevent platelet aggregation along the endothelial surfaces of the microcirculation, and may thereby help to maintain improved perfusion of the injured spinal cord.

Erythropoietin-mediated preservation of the white matter in rat spinal cord injury

Neuroscience ◽  
2007 ◽  
Vol 144 (3) ◽  
pp. 865-877 ◽  
Author(s):  
L. Vitellaro-Zuccarello ◽  
S. Mazzetti ◽  
L. Madaschi ◽  
P. Bosisio ◽  
A. Gorio ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Rat Spinal Cord ◽  
Cord Injury

scholarly journals Dorsal and ventral horn atrophy is associated with clinical outcome after spinal cord injury

Neurology ◽  
2018 ◽  
Vol 90 (17) ◽  
pp. e1510-e1522 ◽  
Author(s):  
Eveline Huber ◽  
Gergely David ◽  
Alan J. Thompson ◽  
Nikolaus Weiskopf ◽  
Siawoosh Mohammadi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Clinical Outcome ◽  
Gray Matter ◽  
Ventral Horn ◽  
Tissue Specific ◽  
Weighted Sequence ◽  
Cord Injury ◽  
Lesion Severity

ObjectiveTo investigate whether gray matter pathology above the level of injury, alongside white matter changes, also contributes to sensorimotor impairments after spinal cord injury.MethodsA 3T MRI protocol was acquired in 17 tetraplegic patients and 21 controls. A sagittal T2-weighted sequence was used to characterize lesion severity. At the C2-3 level, a high-resolution T2*-weighted sequence was used to assess cross-sectional areas of gray and white matter, including their subcompartments; a diffusion-weighted sequence was used to compute voxel-based diffusion indices. Regression models determined associations between lesion severity and tissue-specific neurodegeneration and associations between the latter with neurophysiologic and clinical outcome.ResultsNeurodegeneration was evident within the dorsal and ventral horns and white matter above the level of injury. Tract-specific neurodegeneration was associated with prolonged conduction of appropriate electrophysiologic recordings. Dorsal horn atrophy was associated with sensory outcome, while ventral horn atrophy was associated with motor outcome. White matter integrity of dorsal columns and corticospinal tracts was associated with daily-life independence.ConclusionOur results suggest that, next to anterograde and retrograde degeneration of white matter tracts, neuronal circuits within the spinal cord far above the level of injury undergo transsynaptic neurodegeneration, resulting in specific gray matter changes. Such improved understanding of tissue-specific cord pathology offers potential biomarkers with more efficient targeting and monitoring of neuroregenerative (i.e., white matter) and neuroprotective (i.e., gray matter) agents.

scholarly journals Vascular mechanisms in the pathophysiology of human spinal cord injury

1997 ◽  
Vol 2 (1) ◽  
pp. E2
Author(s):  
Charles H. Tator ◽  
Izumi Koyanagi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Gray Matter ◽  
White Matter Lesions ◽  
Arterial System ◽  
Secondary Injury ◽  
Human Spinal Cord ◽  
Injury Mechanisms ◽  
Cord Injury

Vascular injury plays an important role in the primary and secondary injury mechanisms that cause damage to the acutely traumatized spinal cord. To understand the pathophysiology of human spinal cord injury, the authors investigated the vascular system in three uninjured human spinal cords using silicone rubber microangiography and analyzed the histological findings related to vascular injury in nine acutely traumatized human spinal cords obtained at autopsy. The interval from spinal cord injury to death ranged from 20 minutes to 9 months. The microangiograms of the uninjured human cervical cords demonstrated new information about the sulcal arterial system and the pial arteries. The centrifugal sulcal arterial system was found to supply all of the anterior gray matter, the anterior half of the posterior gray matter, approximately the inner half of the anterior and lateral white columns, and the anterior half of the posterior white columns. Traumatized spinal cord specimens in the acute stage (3-5 days postinjury) showed severe hemorrhages predominantly in the gray matter, but also in the white matter. The white matter surrounding the hemorrhagic gray matter showed a variety of lesions, including decreased staining, disrupted myelin, and axonal and periaxonal swelling. The white matter lesions extended far from the injury site, especially in the posterior columns. There was no evidence of complete occlusion of any of the larger arteries, including the anterior and posterior spinal arteries and the sulcal arteries. However, occluded intramedullary veins were identified in the degenerated posterior white columns. In the chronic stage (3-9 months postinjury), the injured segments showed major tissue loss with large cavitations, whereas both rostral and caudal remote sites showed well-demarcated necrotic areas indicative of infarction mainly in the posterior white columns. Obstruction of small intramedullary arteries and veins by the initial mechanical stress or secondary injury mechanisms most likely produced these extensive white matter lesions. Our studies implicate damage to the anterior sulcal arteries in causing the hemorrhagic necrosis and subsequent central myelomalacia at the injury site in acute spinal cord injury in humans.

Effect of acute spinal cord compression injury on regional spinal cord blood flow in primates

1976 ◽  
Vol 45 (6) ◽  
pp. 660-676 ◽  
Author(s):  
Alan N. Sandler ◽  
Charles H. Tator
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
White Matter ◽  
Cord Blood ◽  
Gray Matter ◽  
Regional Blood Flow ◽  
Compression Injury ◽  
Spinal Cord Blood Flow ◽  
Content Type ◽  
Cord Injury

✓ Spinal cord blood flow (SCBF) was measured in 24 rhesus monkeys after injury to the cord produced by the inflatable circumferential extradural cuff technique. Measurement of regional blood flow in the white and gray matter of the cord in areas of 0.1 sq mm was achieved with the 14C-antipyrine autoradiographic technique and a scanning microscope photometer. After moderate cord injury (400 mm Hg pressure in the cuff maintained for 5 minutes), which produced paraplegia in 50% of animals and moderate to severe paresis in the other 50%, mean white matter SCBF was significantly decreased for up to 1 hour. White matter blood flow then rose to normal levels by 6 hours posttrauma and was significantly increased by 24 hours posttrauma. Gray matter SCBF was significantly decreased for the entire 24-hour period post-trauma. After severe cord injury (150 mm Hg pressure in the cuff maintained for 3 hours), which produced total paraplegia in almost all animals, SCBF in white and gray matter was reduced to extremely low levels for 24 hours posttrauma. In addition, focal decreases in SCBF were seen in white and gray matter for considerable distances proximal and distal to the injury site. It is concluded that acute compression injury of the spinal cord is associated with long-lasting ischemia in the cord that increases in severity with the degree of injury.

scholarly journals Feasibility of Diffusion Kurtosis Imaging in Evaluating Cervical Spinal Cord Injury in Multiple Sclerosis

2022 ◽  
Author(s):  
BingYang Bian ◽  
ZhuoHang Liu ◽  
ZhiQing Shao ◽  
Pu Tian ◽  
YaQian Liang ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
White Matter ◽  
Therapeutic Effect ◽  
Gray Matter ◽  
Cervical Spinal Cord ◽  
Diffusion Kurtosis Imaging ◽  
Cord Injury ◽  
Before And After ◽  
Diffusion Kurtosis

Abstract Background：Quantitative evaluation of cervical spinal cord (CSC) injury in multiple sclerosis has always been a difficulty. The present study aimed to evaluate the lesion, normal-appearing gray matter (GM) and white matter (WM) damage, and therapeutic effect using diffusion kurtosis imaging (DKI) on CSC of patients with multiple sclerosis.Methods: A total of 48 patients with MS and 30 healthy adults, underwent routine MR scan and DKI of CSC. DKI-metrics were measured in the lesions and in the normal-appearing gray and white matter. MS patients were divided into those with and without T2-hyperintense lesions. Disability was assessed by the expanded disability status scale before and after therapy.Results：1) Significant differences were detected in MK, MD, and FA values between patients and healthy subjects (P < 0.05) and between patients with CSC T2-hyperintense and patients without T2-hyperintense (P < 0.05); 2) Compared to healthy, GM-MK and WM-FA were statistically reduced in patients without T2-hyperintense (P < 0.05). 3) Significant differences were observed in MK, MD, and FA between patients with T2-hyperintense after therapy (P < 0.05), as well as GM-MK and WM-FA in patients without T2-hyperintense (P < 0.05); 4) EDSS was correlated with MK values, as well as EDSS scores and MK values after therapy.Conclusions：1) DKI-metrics can detect and quantitatively evaluate the changes in cervical spinal cord micropathological structure; 2) MK values are sensitive metrics to detect the damage of gray matter; 3) MK values quantitatively evaluate the clinical disability progression and the therapeutic effect in MS patients.

Vascular mechanisms in the pathophysiology of human spinal cord injury

1997 ◽  
Vol 86 (3) ◽  
pp. 483-492 ◽  
Author(s):  
Charles H. Tator ◽  
Izumi Koyanagi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Gray Matter ◽  
White Matter Lesions ◽  
Arterial System ◽  
Secondary Injury ◽  
Human Spinal Cord ◽  
Injury Mechanisms ◽  
Cord Injury

✓ Vascular injury plays an important role in the primary and secondary injury mechanisms that cause damage to the acutely traumatized spinal cord. To understand the pathophysiology of human spinal cord injury, the authors investigated the vascular system in three uninjured human spinal cords using silicone rubber microangiography and analyzed the histological findings related to vascular injury in nine acutely traumatized human spinal cords obtained at autopsy. The interval from spinal cord injury to death ranged from 20 minutes to 9 months. The microangiograms of the uninjured human cervical cords demonstrated new information about the sulcal arterial system and the pial arteries. The centrifugal sulcal arterial system was found to supply all of the anterior gray matter, the anterior half of the posterior gray matter, approximately the inner half of the anterior and lateral white columns, and the anterior half of the posterior white columns. Traumatized spinal cord specimens in the acute stage (3–5 days postinjury) showed severe hemorrhages predominantly in the gray matter, but also in the white matter. The white matter surrounding the hemorrhagic gray matter showed a variety of lesions, including decreased staining, disrupted myelin, and axonal and periaxonal swelling. The white matter lesions extended far from the injury site, especially in the posterior columns. There was no evidence of complete occlusion of any of the larger arteries, including the anterior and posterior spinal arteries and the sulcal arteries. However, occluded intramedullary veins were identified in the degenerated posterior white columns. In the chronic stage (3–9 months postinjury), the injured segments showed major tissue loss with large cavitations, whereas both rostral and caudal remote sites showed well-demarcated necrotic areas indicative of infarction mainly in the posterior white columns. Obstruction of small intramedullary arteries and veins by the initial mechanical stress or secondary injury mechanisms most likely produced these extensive white matter lesions. Our studies implicate damage to the anterior sulcal arteries in causing the hemorrhagic necrosis and subsequent central myelomalacia at the injury site in acute spinal cord injury in humans.

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