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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Autor principal: González, S.
Otros Autores: Labombarda, F., Gonzalez Deniselle, M.C, Saravia, F.E, Roig, P., De Nicola, A.F
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2001
Acceso en línea:Registro en Scopus
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024 7 |2 scopus  |a 2-s2.0-0035823376 
024 7 |2 cas  |a Dexamethasone, 50-02-2; Glucocorticoids; NADPH Dehydrogenase, EC 1.6.99.1; Nitric Oxide, 10102-43-9; Proto-Oncogene Proteins c-fos 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a BRREA 
100 1 |a González, S. 
245 1 0 |a Glucocorticoid effects on Fos immunoreactivity and NADPH-diaphorase histochemical staining following spinal cord injury 
260 |c 2001 
270 1 0 |m De Nicola, A.F.; Lab. of Neuroendocrine Biochemistry, Instituto de Biología, Obligado 2490, 1428 Buenos Aires, Argentina; email: denicola@proteus.dna.uba.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a 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.  |l eng 
536 |a Detalles de la financiación: Universidad de Buenos Aires, MT13 
536 |a Detalles de la financiación: Fondo para la Investigación Científica y Tecnológica, BID 802 OC AR PICT 97 05-00438 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas, PEI 03228/98, PIP 4103 
536 |a Detalles de la financiación: This work was supported by grants from CONICET (PIP 4103 and PEI 03228/98), University of Buenos Aires (MT13), FONCYT (BID 802 OC AR PICT 97 05-00438), Fundación Barceló (Buenos Aires) and Beca Ramón Carrillo-Arturo Oñativia from the Minister of Health of Argentina. 
593 |a Laboratory of Neuroendocrine Biochemistry, Instituto de Biología y Medicina Experimental, Obligado 2490, 1428 Buenos Aires, Argentina 
593 |a Department of Human Biochemistry, Faculty of Medicine, University of Buenos Aires, Buenos Aires, Argentina 
593 |a Instituto Universitario de Ciencias de la Salud, Fundación Barceló, Buenos Aires, Argentina 
690 1 0 |a DEXAMETHASONE 
690 1 0 |a FOS 
690 1 0 |a GLOCOCORTICOID 
690 1 0 |a NADPH-DIAPHORASE 
690 1 0 |a NEUROPROTECTION 
690 1 0 |a SPINAL CORD INJURY 
690 1 0 |a DEXAMETHASONE 
690 1 0 |a GLUCOCORTICOID 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a PROTEIN FOS 
690 1 0 |a REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE DEHYDROGENASE 
690 1 0 |a ADRENERGIC SYSTEM 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL MODEL 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a CELL ACTIVATION 
690 1 0 |a CELL COUNT 
690 1 0 |a CELL POPULATION 
690 1 0 |a COMPUTER ANALYSIS 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DOSE TIME EFFECT RELATION 
690 1 0 |a DOWN REGULATION 
690 1 0 |a IMAGE ANALYSIS 
690 1 0 |a IMMUNOCOMPETENT CELL 
690 1 0 |a IMMUNOHISTOCHEMISTRY 
690 1 0 |a IMMUNOREACTIVITY 
690 1 0 |a MALE 
690 1 0 |a NERVE POTENTIAL 
690 1 0 |a NOCICEPTION 
690 1 0 |a NONHUMAN 
690 1 0 |a PAIN 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a PROTEIN EXPRESSION 
690 1 0 |a PROTEIN INDUCTION 
690 1 0 |a RAT 
690 1 0 |a SPINAL CORD DORSAL HORN 
690 1 0 |a SPINAL CORD INJURY 
690 1 0 |a SPINAL CORD TRANSSECTION 
690 1 0 |a THORACIC SPINAL CORD 
690 1 0 |a TIME 
690 1 0 |a VERTEBRAL CANAL 
690 1 0 |a ANIMALS 
690 1 0 |a CELL COUNT 
690 1 0 |a DEXAMETHASONE 
690 1 0 |a DOSE-RESPONSE RELATIONSHIP, DRUG 
690 1 0 |a DOWN-REGULATION 
690 1 0 |a DRUG ADMINISTRATION SCHEDULE 
690 1 0 |a GLUCOCORTICOIDS 
690 1 0 |a IMMUNOHISTOCHEMISTRY 
690 1 0 |a MALE 
690 1 0 |a NADPH DEHYDROGENASE 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a PAIN 
690 1 0 |a PROTO-ONCOGENE PROTEINS C-FOS 
690 1 0 |a RATS 
690 1 0 |a RATS, SPRAGUE-DAWLEY 
690 1 0 |a SPINAL CORD INJURIES 
690 1 0 |a SUBSTANTIA GELATINOSA 
690 1 0 |a TIME FACTORS 
690 1 0 |a UP-REGULATION 
700 1 |a Labombarda, F. 
700 1 |a Gonzalez Deniselle, M.C. 
700 1 |a Saravia, F.E. 
700 1 |a Roig, P. 
700 1 |a De Nicola, A.F. 
773 0 |d 2001  |g v. 912  |h pp. 144-153  |k n. 2  |p Brain Res.  |x 00068993  |w (AR-BaUEN)CENRE-4052  |t Brain Research 
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