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  • 1
    Electronic Resource
    Electronic Resource
    Edema formation and cellular alterations following spinal cord injury in the rat and their modification with p-chlorophenylalanine (1990)
    Springer
    Acta neuropathologica 79 (1990), S. 604-610 
    Details
    ISSN: 1432-0533
    Keywords: Trauma ; Spinal cord injury ; Edema ; Serotonin ; p-CPA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that serotonin can modify the early pathological sequences occurring in spinal cord trauma was investigated in a rat model. To that end we took advantage of the possibility of influencing serotonin pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA) before the production of the injury and compared the results with injured, untreated controls. A unilateral incision was made into the dorsal horn of the lower thoracic cord (about 2.5 mm deep, 4.5 mm long) and the trauma. The injured region from untreated animals showed macroscopically at that time a pronounced swelling and the water content had increased by 3.5% as compared to intact controls. The segments rostral and caudal to the lesion also exhibited a profound increase in water content. Light microscopy revealed a significant expansion of the spinal cord as compared to controls. The swelling was most pronounced in the gray matter on the injured side. Electron microscopy showed distorted neurons, swollen astrocytes and extracellular edema in the gray matter in and around the primary lesion. There was also a sponginess in the surrounding white matter with disruption of myelin, collapsed axons and widened periaxonal spaces. Pretreatment of the rats with p-CPA significantly reduced the swelling of the injured spinal cord and there was no visible expansion. The ipsilateral edema in the central gray matter was considerable less pronounced as compared to that in untreated animals. The increase in water content was less than 1% in these animals. The neuronal and glial cell changes were also markedly reduced in the drugtreated rats. The disruption of myelin and the vacuolation of the gray matter were much less severe. Our results show that p-CPA can markedly modify the edema and the cellular changes occurring in the traumatic spinal injury and indicate that serotonin is somehow involved in the production of the early, and thus important, pathological events.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294237
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of p-chlorophenylalanine on microvascular permeability changes in spinal cord trauma (1990)
    Springer
    Acta neuropathologica 79 (1990), S. 595-603 
    Details
    ISSN: 1432-0533
    Keywords: Trauma ; Spinal cord injury ; Microvascular permeability ; Serotonin ; p-Chlorophenylalanine (p-CPA)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that serotonin can take part in the initiation of the increased microvascular permeability occurring in a spinal cord trauma was investigated in a rat model with 131I-sodium and lanthanum as tracers. We influenced the serotonin content in the tissue pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA), before the production of the injury and compared the results with injured, untreated controls. A small incision was made in the dorsal horn of the lower thoracic cord. It caused a progressive extravasation of 131I-sodium in the damaged segment, measured after 1,2 and 5 h. Rostral and caudal segments also showed a significant but lower accumulation of 131I-sodium. Lanthanum added to the fixative was used as an ionic tracer detectable by electron microscopy. The endothelial cells of microvessels removed from the perifocal region after 5 h showed a marked increase in the number of lanthanum-filled vesicles. Many endothelial cells had a diffuse penetration of the tracer into the cytoplasm and the basement membrane. However, the tight junctions usually remained closed to lanthanum. Pretreatment with p-CPA markedly reduced the extravasation of 131I-sodium measured at 5 h in the traumatized cord. At the cellular level, the endothelial vesicles filled with lanthanum approached the condition of uninjured animals. The diffuse infiltration of lanthanum into endothelial cells and its spread into the basement membrane of the vascular wall were usually absent. Our results indicate that serotonin plays a role in the initiation of the increased microvascular permeability which occurs in spinal cord injuries.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294236
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Brain derived neurotrophic factor and insulin like growth factor-1 attenuate upregulation of nitric oxide synthase and cell injury following trauma to the spinal cord (1998)
    Springer
    Amino acids 14 (1998), S. 121-129 
    Details
    ISSN: 1438-2199
    Keywords: Brain derived neurotrophic factor ; Insulin like growth factor-1 ; Nitric oxide ; Spinal cord injury ; Edema ; Cell injury ; Blood-spinal cord barrier ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possibility that brain derived neurotrophic factor (BDNF) and insulin like growth factor-1 (IGF) induced neuroprotectivn is influenced by mechanisms involving nitric oxide was examined in a rat model of focal spinal cord injury. BDNF or IGF-I (0.1 μg/10 [1 in phosphate buffer saline) was applied topically 30 min before injury on the exposed spinal cord followed by repeated doses of growth factors immediately before and 30 min after injury. Thereafter application of BDNF or IGF was carried out at every 1 h interval until sacrifice. Five hours after injury, the tissue pieces from the T9 segment were processed for nNOS immunostaining, edema and cell injury. Untreated injured rats showed a profound upregulation of nNOS which was most pronounced in the nerve cells of the ipsilateral side. A marked increase in the blood-spinal cord barrier (BSCB) permeability to125I-albumin, water content and cell injury in these perifocal segments was also found. Pretreatment with BDNF and IGF significantly reduced the upregulation of nNOS in the spinal cord. This effect of the growth factors was most pronounced in the contralateral side. Rats treated with these neurotrophic factors showed much less signs of BSCB damage, edema and cell injury. These results suggest that BDNF and IGF pretreatment is neuroprotective in spinal cord injury and that these neurotrophic factors have the capacity to down regulate nNOS expression following trauma to the spinal cord. Our data provide new experimental evidences which suggest that BDNF and IGF may exert their potential neuroprotective effects probably via regulation of NOS activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01345252
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Neurotrophic factors influence upregulation of constitutive isoform of heme oxygenase and cellular stress response in the spinal cord following trauma (2000)
    Springer
    Amino acids 19 (2000), S. 351-361 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Spinal cord injury ; Heme oxygenase ; Heat shock protein ; Carbon monoxide ; Growth factors ; BDNF ; IGF-1 ; Immunohistochemistry ; Cell injury ; Spinal cord edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The influence of brain derived neurotrophic factor (BDNF) or insulin like growth factor-1 (IGF-1) on spinal cord trauma induced carbon monoxide (CO) production and cellular stress response was examined using immunostaining of the constitutive isoform of the hemeoxygenase (HO-2) enzyme and the heat shock protein (HSP 72 kD) expression in a rat model. Subjection of rats to a 5 h spinal trauma inflicted by an incision into the right dorsal horn at T10–11 segment markedly upregulated the HO-2 and HSP expression in the adjacent spinal cord segments (T9 and T12). Pretreatment with BDNF or IGF-1 significantly attenuated the trauma induced HSP expression. The upregulation of HO-2 was also considerably reduced. These results show that BDNF and IGF-1 attenuate cellular stress response and production of CO following spinal cord injury which seems to be the key factors in neurotrophins induced neuroprotection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070066
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Growth hormone attenuates alterations in spinal cord evoked potentials and cell injury following trauma to the rat spinal cord (2000)
    Springer
    Amino acids 19 (2000), S. 363-371 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids ; Growth hormone ; Spinal cord injury ; Edema formation ; Spinal cord evoked potentials ; Spinal cord edema ; Cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The influence of exogenous rat growth hormone on spinal cord injury induced alterations in spinal cord evoked potentials (SCEP) and edema formation was examined in a rat model. Repeated topical application of rat growth hormone (20 μl of 1 μg/ml solution) applied 30 min before injuryand at 0 min (at the time of injury), 10 min, 30 min, 60 min, 120 min, 180 min, and 240 min, resulted in a marked preservation of SCEP amplitude after injury. In addition, the treated traumatised cord showed significantly less edema and cell changes. These observations suggest that growth hormone has the capacity to improve spinal cord conduction and attenuate edema formation and cell injury in the cord indicating a potential therapeutic implication of this peptide in spinal cord injuries.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070067
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    Paper (German National Licenses)
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