Glucocorticoid regulation of motoneuronal parameters in rats with spinal cord injury

1. Glucocorticoids exert beneficial effects after acute CNS injury in humans and experimental animals. To elucidate potential mechanisms of glucocorticoid action in the lesioned spinal cord, we have studied if treatment with dexamethasone (DEX) modulated the neurotrophin binding receptor p75 (p75(NT...

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Autor principal: Gonzalez, S.L
Otros Autores: Saravia, F., Gonzalez Deniselle, M.C, Lima, A.E, De Nicola, A.F
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 1999
Acceso en línea:Registro en Scopus
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024 7 |2 scopus  |a 2-s2.0-0033041953 
024 7 |2 cas  |a Choline O-Acetyltransferase, EC 2.3.1.6; Dexamethasone, 50-02-2; Glucocorticoids; Receptor, Nerve Growth Factor; Receptors, Nerve Growth Factor 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a CMNED 
100 1 |a Gonzalez, S.L. 
245 1 0 |a Glucocorticoid regulation of motoneuronal parameters in rats with spinal cord injury 
260 |c 1999 
270 1 0 |m De Nicola, A.F.; Lab. of Neuroendocrine Biochemistry, Inst. de Biol./Medicina Experimental, 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 1. Glucocorticoids exert beneficial effects after acute CNS injury in humans and experimental animals. To elucidate potential mechanisms of glucocorticoid action in the lesioned spinal cord, we have studied if treatment with dexamethasone (DEX) modulated the neurotrophin binding receptor p75 (p75(NTR)) and choline acetyltransferase (ChAT), a marker of neuronal functional viability. 2. Rats with a sham operation or with spinal cord transection at the thoracic level received vehicle or DEX several times postlesion and were sacrificed 48 hr after surgery. The lumbar region caudal to the lesion was processed for p75(NTR) and ChAT immunoreactivity (IR) using quantitative densitometric analysis. 3. We observed that p75(NTR)-IR was absent from ventral horn motoneurons of sham-operated rats, in contrast to strong staining of neuronal perikaryon in TRX rats. Administration of DEX to TRX rats had no effect on the number of neuronal cell bodies expressing p75(NTR)-IR but significantly increased the number and length of immunostained neuronal processes. 4. Furthermore, spinal cord transection reduced ChAT immunostaining of motoneurons by 50%, whereas DEX treatment reverted this pattern to cells with a strong immunoreaction intensity in perikaryon and cell processes. 5. It is hypothesized that increased expression of p75(NTR) in cell processes and of ChAT in motoneurons may be part of a mechanism by which glucocorticoids afford neuroprotection, in addition to their known antiinflammatory effects.  |l eng 
536 |a Detalles de la financiación: Universidad de Buenos Aires, MI3 
536 |a Detalles de la financiación: National Institutes of Health, NS 20866-08 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas, PIP 4103 
536 |a Detalles de la financiación: Fondo para la Investigación Científica y Tecnológica, PICT 00438 
536 |a Detalles de la financiación: This work was supported by grants from the National Institutes of Health (NS 20866-08), the University of Buenos Aires (MI3), CONICET (PIP 4103), Fundación Barceló, and FONCYT (PICT 00438). 
593 |a Lab. of Neuroendocrine Biochemistry, Inst. de Biol. y Med. Experimental, UBA-CONICET, Buenos Aires, Argentina 
593 |a Inst. Univ. de Ciencias de la Salud, Fundación Barceló, Buenos Aires, Argentina 
593 |a Lab. of Neuroendocrine Biochemistry, Inst. de Biol. y Med. Experimental, Obligado 2490, 1428 Buenos Aires, Argentina 
690 1 0 |a CHOLINE ACETYLTRANSFERASE 
690 1 0 |a GLUCOCORTICOIDS 
690 1 0 |a MOTONEURONS 
690 1 0 |a NEUROPROTECTION 
690 1 0 |a P75 NEUROTROPHIN RECEPTOR 
690 1 0 |a SPINAL CORD TRANSECTION 
690 1 0 |a DEXAMETHASONE 
690 1 0 |a GLUCOCORTICOID 
690 1 0 |a NEUROTROPIN 
690 1 0 |a PROTEIN P75 
690 1 0 |a UNCLASSIFIED DRUG 
690 1 0 |a ANIMAL CELL 
690 1 0 |a ANTIINFLAMMATORY ACTIVITY 
690 1 0 |a ARTICLE 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DENSITOMETRY 
690 1 0 |a DRUG MECHANISM 
690 1 0 |a IMMUNOREACTIVITY 
690 1 0 |a MALE 
690 1 0 |a NEUROPROTECTION 
690 1 0 |a NONHUMAN 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a QUANTITATIVE ASSAY 
690 1 0 |a RAT 
690 1 0 |a SPINAL CORD INJURY 
690 1 0 |a SPINAL CORD MOTONEURON 
690 1 0 |a STEROID METABOLISM 
690 1 0 |a SUBCUTANEOUS DRUG ADMINISTRATION 
690 1 0 |a ANIMALS 
690 1 0 |a CHOLINE O-ACETYLTRANSFERASE 
690 1 0 |a DEXAMETHASONE 
690 1 0 |a GLUCOCORTICOIDS 
690 1 0 |a MALE 
690 1 0 |a MOTOR NEURONS 
690 1 0 |a RATS 
690 1 0 |a RATS, SPRAGUE-DAWLEY 
690 1 0 |a RECEPTOR, NERVE GROWTH FACTOR 
690 1 0 |a RECEPTORS, NERVE GROWTH FACTOR 
690 1 0 |a SPINAL CORD INJURIES 
690 1 0 |a ANIMALIA 
700 1 |a Saravia, F. 
700 1 |a Gonzalez Deniselle, M.C. 
700 1 |a Lima, A.E. 
700 1 |a De Nicola, A.F. 
773 0 |d 1999  |g v. 19  |h pp. 597-611  |k n. 5  |p Cell. Mol. Neurobiol.  |x 02724340  |t Cellular and Molecular Neurobiology 
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856 4 0 |u https://doi.org/10.1023/A:1006980301382  |y DOI 
856 4 0 |u https://hdl.handle.net/20.500.12110/paper_02724340_v19_n5_p597_Gonzalez  |y Handle 
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