Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury

Glucocorticoids (GC) provide neuroprotection and early recovery after spinal cord injury (SCI). While several mechanisms were proposed to account for these effects, limited information exists regarding GC actions in sensory areas of the spinal cord. Presently, we studied the time course of Fos expre...

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Autores principales: González, S., Labombarda, F., Gonzalez Deniselle, M.C., Saravia, F.E., Roig, P., De Nicola, A.F.
Formato: JOUR
Materias:
Fos
rat
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_00068993_v912_n2_p144_Gonzalez
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spelling todo:paper_00068993_v912_n2_p144_Gonzalez2023-10-03T14:05:24Z Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury González, S. Labombarda, F. Gonzalez Deniselle, M.C. Saravia, F.E. Roig, P. De Nicola, A.F. Dexamethasone Fos Glococorticoid NADPH-diaphorase Neuroprotection Spinal cord injury dexamethasone glucocorticoid nitric oxide protein fos reduced nicotinamide adenine dinucleotide phosphate dehydrogenase adrenergic system animal experiment animal model animal tissue article cell activation cell count cell population computer analysis controlled study dose time effect relation down regulation image analysis immunocompetent cell immunohistochemistry immunoreactivity male nerve potential nociception nonhuman pain priority journal protein expression protein induction rat spinal cord dorsal horn spinal cord injury spinal cord transsection thoracic spinal cord time vertebral canal Animals Cell Count Dexamethasone Dose-Response Relationship, Drug Down-Regulation Drug Administration Schedule Glucocorticoids Immunohistochemistry Male NADPH Dehydrogenase Nitric Oxide Pain Proto-Oncogene Proteins c-fos Rats Rats, Sprague-Dawley Spinal Cord Injuries Substantia Gelatinosa Time Factors Up-Regulation Glucocorticoids (GC) provide neuroprotection and early recovery after spinal cord injury (SCI). While several mechanisms were proposed to account for these effects, limited information exists regarding GC actions in sensory areas of the spinal cord. Presently, we studied the time course of Fos expression, and reduced nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical staining to monitor neuronal responses to SCI with or without GC treatment. Rats with sham-operation or transection at the thoracic level (T7-T8) received vehicle or 5 mg/kg of the GC dexamethasone (DEX) at 5 min post-lesion and were sacrificed 2 or 4 h after surgery. Another group of SCI rats received vehicle or intensive DEX treatment (5 min, 6 h, 18 h and 46 h post-lesion) and were sacrificed 48 h after surgery. The number of NADPH-d positive neurons or Fos immunoreactive nuclei was studied by computer-assisted image analysis in superficial dorsal horn (Laminae I-III) and central canal area (Lamina X) below the lesion. While constitutive Fos immunoreactive nuclei were sparse in controls, SCI increased Fos expression at 2 and 4 h after injury. DEX treatment significantly enhanced the number of Fos positive nuclei in Laminae I-III by 4 h after transection, although the response was not maintained by intensive steroid treatment when tested at 48 h after SCI. NADPH-d positive neurons in Laminae I-III increased at 2 and 4 h after SCI while a delayed increased was found in central canal area (Lamina X). DEX treatment decreased NADPH-d positive neurons to sham-operated levels at all time points examined. Thus, while GC stimulation of Fos suggests activation of neurons involved in sympathetic outflow and/or pain, down-regulation of NADPH-d indicates attenuation of nociceptive outflow, considering the role of enzyme-derived nitric oxide in pain-related mechanisms. Differential hormonal effects on these molecules agree with their localization in different cell populations. © 2001 Elsevier Science B.V. All rights reserved. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00068993_v912_n2_p144_Gonzalez
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Dexamethasone
Fos
Glococorticoid
NADPH-diaphorase
Neuroprotection
Spinal cord injury
dexamethasone
glucocorticoid
nitric oxide
protein fos
reduced nicotinamide adenine dinucleotide phosphate dehydrogenase
adrenergic system
animal experiment
animal model
animal tissue
article
cell activation
cell count
cell population
computer analysis
controlled study
dose time effect relation
down regulation
image analysis
immunocompetent cell
immunohistochemistry
immunoreactivity
male
nerve potential
nociception
nonhuman
pain
priority journal
protein expression
protein induction
rat
spinal cord dorsal horn
spinal cord injury
spinal cord transsection
thoracic spinal cord
time
vertebral canal
Animals
Cell Count
Dexamethasone
Dose-Response Relationship, Drug
Down-Regulation
Drug Administration Schedule
Glucocorticoids
Immunohistochemistry
Male
NADPH Dehydrogenase
Nitric Oxide
Pain
Proto-Oncogene Proteins c-fos
Rats
Rats, Sprague-Dawley
Spinal Cord Injuries
Substantia Gelatinosa
Time Factors
Up-Regulation
spellingShingle Dexamethasone
Fos
Glococorticoid
NADPH-diaphorase
Neuroprotection
Spinal cord injury
dexamethasone
glucocorticoid
nitric oxide
protein fos
reduced nicotinamide adenine dinucleotide phosphate dehydrogenase
adrenergic system
animal experiment
animal model
animal tissue
article
cell activation
cell count
cell population
computer analysis
controlled study
dose time effect relation
down regulation
image analysis
immunocompetent cell
immunohistochemistry
immunoreactivity
male
nerve potential
nociception
nonhuman
pain
priority journal
protein expression
protein induction
rat
spinal cord dorsal horn
spinal cord injury
spinal cord transsection
thoracic spinal cord
time
vertebral canal
Animals
Cell Count
Dexamethasone
Dose-Response Relationship, Drug
Down-Regulation
Drug Administration Schedule
Glucocorticoids
Immunohistochemistry
Male
NADPH Dehydrogenase
Nitric Oxide
Pain
Proto-Oncogene Proteins c-fos
Rats
Rats, Sprague-Dawley
Spinal Cord Injuries
Substantia Gelatinosa
Time Factors
Up-Regulation
González, S.
Labombarda, F.
Gonzalez Deniselle, M.C.
Saravia, F.E.
Roig, P.
De Nicola, A.F.
Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury
topic_facet Dexamethasone
Fos
Glococorticoid
NADPH-diaphorase
Neuroprotection
Spinal cord injury
dexamethasone
glucocorticoid
nitric oxide
protein fos
reduced nicotinamide adenine dinucleotide phosphate dehydrogenase
adrenergic system
animal experiment
animal model
animal tissue
article
cell activation
cell count
cell population
computer analysis
controlled study
dose time effect relation
down regulation
image analysis
immunocompetent cell
immunohistochemistry
immunoreactivity
male
nerve potential
nociception
nonhuman
pain
priority journal
protein expression
protein induction
rat
spinal cord dorsal horn
spinal cord injury
spinal cord transsection
thoracic spinal cord
time
vertebral canal
Animals
Cell Count
Dexamethasone
Dose-Response Relationship, Drug
Down-Regulation
Drug Administration Schedule
Glucocorticoids
Immunohistochemistry
Male
NADPH Dehydrogenase
Nitric Oxide
Pain
Proto-Oncogene Proteins c-fos
Rats
Rats, Sprague-Dawley
Spinal Cord Injuries
Substantia Gelatinosa
Time Factors
Up-Regulation
description Glucocorticoids (GC) provide neuroprotection and early recovery after spinal cord injury (SCI). While several mechanisms were proposed to account for these effects, limited information exists regarding GC actions in sensory areas of the spinal cord. Presently, we studied the time course of Fos expression, and reduced nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical staining to monitor neuronal responses to SCI with or without GC treatment. Rats with sham-operation or transection at the thoracic level (T7-T8) received vehicle or 5 mg/kg of the GC dexamethasone (DEX) at 5 min post-lesion and were sacrificed 2 or 4 h after surgery. Another group of SCI rats received vehicle or intensive DEX treatment (5 min, 6 h, 18 h and 46 h post-lesion) and were sacrificed 48 h after surgery. The number of NADPH-d positive neurons or Fos immunoreactive nuclei was studied by computer-assisted image analysis in superficial dorsal horn (Laminae I-III) and central canal area (Lamina X) below the lesion. While constitutive Fos immunoreactive nuclei were sparse in controls, SCI increased Fos expression at 2 and 4 h after injury. DEX treatment significantly enhanced the number of Fos positive nuclei in Laminae I-III by 4 h after transection, although the response was not maintained by intensive steroid treatment when tested at 48 h after SCI. NADPH-d positive neurons in Laminae I-III increased at 2 and 4 h after SCI while a delayed increased was found in central canal area (Lamina X). DEX treatment decreased NADPH-d positive neurons to sham-operated levels at all time points examined. Thus, while GC stimulation of Fos suggests activation of neurons involved in sympathetic outflow and/or pain, down-regulation of NADPH-d indicates attenuation of nociceptive outflow, considering the role of enzyme-derived nitric oxide in pain-related mechanisms. Differential hormonal effects on these molecules agree with their localization in different cell populations. © 2001 Elsevier Science B.V. All rights reserved.
format JOUR
author González, S.
Labombarda, F.
Gonzalez Deniselle, M.C.
Saravia, F.E.
Roig, P.
De Nicola, A.F.
author_facet González, S.
Labombarda, F.
Gonzalez Deniselle, M.C.
Saravia, F.E.
Roig, P.
De Nicola, A.F.
author_sort González, S.
title Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury
title_short Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury
title_full Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury
title_fullStr Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury
title_full_unstemmed Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury
title_sort glucocorticoid effects on fos immunoreactivity and nadph-diaphorase histochemical staining following spinal cord injury
url http://hdl.handle.net/20.500.12110/paper_00068993_v912_n2_p144_Gonzalez
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AT labombardaf glucocorticoideffectsonfosimmunoreactivityandnadphdiaphorasehistochemicalstainingfollowingspinalcordinjury
AT gonzalezdenisellemc glucocorticoideffectsonfosimmunoreactivityandnadphdiaphorasehistochemicalstainingfollowingspinalcordinjury
AT saraviafe glucocorticoideffectsonfosimmunoreactivityandnadphdiaphorasehistochemicalstainingfollowingspinalcordinjury
AT roigp glucocorticoideffectsonfosimmunoreactivityandnadphdiaphorasehistochemicalstainingfollowingspinalcordinjury
AT denicolaaf glucocorticoideffectsonfosimmunoreactivityandnadphdiaphorasehistochemicalstainingfollowingspinalcordinjury
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