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  • 1
    Electronic Resource
    Electronic Resource
    p-Chlorophenylalanine, a serotonin synthesis inhibitor, reduces the response of glial fibrillary acidic protein induced by trauma to the spinal cord (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 422-427 
    Details
    ISSN: 1432-0533
    Keywords: Spinal cord trauma ; Glial fibrillary acidic protein ; Serotonin ; p-Chlorophenylalanine ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The possibility that serotonin may influence the early response of astrocytes around a spinal cord trauma was investigated in a rat model by making a unilateral incision into the right dorsal horn of the T10-11 segments. One group of rats received a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA) before injury in doses which cause a depletion of serotonin in the cord. Another group of traumatised rats did not receive p-CPA. All animals were allowed to survive for 5 h. Samples for immunohistochemistry were taken from the T9, T10-11 and T12 segments of the cord. Paraffin sections were immunostained for glial fibrillary acidic protein (GFAP) using monoclonal antibodies and avidin-biotin complex technique. Trauma to the cord resulted in a marked increase of GFAP immunoreactivity in all the investigated segments, particularly in the ipsilateral side. Pretreatment with p-CPA markedly reduced the GFAP response. This drug did not by itself influence the GFAP immunoreactivity of the cord of untraumatised rats. Our results show that trauma to the spinal cord induces a rapid enhancement of GFAP immunoreactivity in the cord which is present even far away from the primary lesion. This response can be prevented by pretreatment with the serotonin synthesis inhibitor, p-CPA. The results indicate that serotonin influences the increase of GFAP immunoreactivity following spinal cord injury either directly or indirectly, for instance by its microvascular reactions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00228575
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  • 2
    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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    Paper (German National Licenses)
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  • 3
    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
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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