Estradiol increases glucocorticoid binding and glucocorticoid induction of ornithine decarboxylase in the rat spinal cord

Previous results demonstrated that estradiol (E2) treatment of ovariectomized-adrenalectomized (OVX-ADX) rats increased glucocorticoid (GC) binding in brain regions. The experimental protocol was extended to the spinal cord, a GC target tissue in which ornithine decarboxylase (ODC) is markedly induc...

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Autor principal: Ferrini, M.
Otros Autores: González, S., De Nicola, A.F
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 1993
Acceso en línea:Registro en Scopus
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Registro en la Biblioteca Digital
Aporte de:Registro referencial: Solicitar el recurso aquí
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024 7 |2 scopus  |a 2-s2.0-0027397541 
024 7 |2 cas  |a Estradiol, 50-28-2; Glucocorticoids; Ornithine Decarboxylase, EC 4.1.1.17; Receptors, Glucocorticoid 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a LIFSA 
100 1 |a Ferrini, M. 
245 1 0 |a Estradiol increases glucocorticoid binding and glucocorticoid induction of ornithine decarboxylase in the rat spinal cord 
260 |c 1993 
270 1 0 |m Ferrini, M.; Laboratorio de Bioquímica Neuroendócrina, Instituto de Biología y Medicina Experimental, Obligado 2490, 1428 Buenos Aires, Argentina 
506 |2 openaire  |e Política editorial 
504 |a Mcewen, Brinton, Chao, Coirini, Gannon, Gould, Callaghan, Wooley, (1990) Neuroendocrine Perspectives, pp. 93-130. , E.E. Muller, R.M. Macleod, Springer-Verlag, Berlin 
504 |a Turner, Weaver, (1985) Brain Res., 343, pp. 16-23 
504 |a Turner, (1990) Life Sci., 46, pp. 1399-1406 
504 |a Pfeiffer, Bardin, (1988) Mol. Cell. Endocrinol., 55, pp. 115-120 
504 |a Ferrini, Magariños, De Nicola, J. Steroid Biochem. (1989) J. Steroid Biochem., 50, pp. 673-678 
504 |a Ferrini, De Nicola, (1991) Life Sci., 48, pp. 2593-2601 
504 |a Reul, De Kloet, (1985) Endocrinology, 117, pp. 2502-2511 
504 |a Burgess, Handa, (1990) Soc. Neurosci. Abstr., 16, p. 1070 
504 |a Turner, (1992) Brain Res., 581, pp. 229-236 
504 |a De Nicola, Moses, Gonzalez, Orti, (1989) Cell Mol. Neurobiol., 9, pp. 179-192 
504 |a Orti, Moses, Grillo, De Nicola, (1987) J. Neurochem., 48, pp. 425-431 
504 |a Gonzalez, Moses, De Nicola, (1990) J. Neurochem., 54, pp. 834-840 
504 |a Maclusky, Roy, Shanabrough, Eisenfeld, (1986) J. Neurosci. Methods, 16, pp. 131-140 
504 |a Moses, Orti, De Nicola, (1987) Brain Res., 408, pp. 118-124 
504 |a Palkovits, Brownstein, (1988) Maps and Guide to microdissection of the Rat Brain, , Elsevier, N.Y 
504 |a Magariños, Ferrini, De Nicola, (1989) Neuroendocrinology, 50, pp. 673-678 
504 |a Lowry, Rosebrough, Farr, Randall, (1951) J. Biol. Chem., 193, pp. 265-275 
504 |a Weisenberg, De Nicola, Arakelian, Libertun, (1979) Endocrinology, 105, pp. 1552-1557 
504 |a Russell, Snyder, (1968) Proc. Natl. Acad. Sci. U.S.A., 60, pp. 1420-1427. , Second Edition 
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504 |a Cintra, Fuxe, Agnati, Persson, Harfstrand, Zoli, Eneroth, Zini, (1987) Neurosci. Lett., 76, pp. 269-274 
504 |a Gould, Wooley, Ewen, (1990) Neurosci., 37, pp. 367-375 
504 |a A.F.DE NICOLA, in: Neural Regeneration (F. S. SEIL, ed.) Raven Press, New York (in press); Kanje, Fransson, Edstrom, Lowkvist, (1986) Brain Res, 381, pp. 24-28 
504 |a Soifer, Moretto, Spencer, Sabri, Axotomy-induced ornithine decarboxylase activity in the mouse dorsal root ganglion is inhibited by the vinca alkaloids (1988) Neurochemical Research, 13, pp. 1169-1173 
520 3 |a Previous results demonstrated that estradiol (E2) treatment of ovariectomized-adrenalectomized (OVX-ADX) rats increased glucocorticoid (GC) binding in brain regions. The experimental protocol was extended to the spinal cord, a GC target tissue in which ornithine decarboxylase (ODC) is markedly induced by GC treatment. First, we measured GC binding to type I and type II receptors in ventral horn, dorsal horn and lateral funiculus of OVX-ADX rats treated during 4 days with E2 or vehicle. In E2-treated rats, type II receptors increased solely in dorsal horn, whereas type I sites remained unchanged. Second, in a group of OVX-ADX rats receiving dexamethasone (DEX), pretreatment with E2 superinduced ODC in ventral horn and lateral funiculus, but not in dorsal horn. Third, we found that the dorsal horn was relatively enriched in E2 receptors compared to other areas. Therefore, E2 stimulation of GC binding to type II sites may be mediated through E2 receptors localized in the dorsal horn. We suggest that combined treatment with E2 and DEX employs a transsynaptic mechanism for ODC induction at the ventral horn and lateral funiculus, with hormonal interaction taking place at the dorsal horn level. © 1993.  |l eng 
536 |a Detalles de la financiación: This work was supported by a grant from N.I.H. (NS 20866-06AI) and by the National Research Council of Argentina (PID 3-010200/88). 
593 |a Laboratorio de Bioquímica Neuroendócrina, Instituto de Biología y Medicina Experimental, Obligado 2490, 1428 Buenos Aires, Argentina 
690 1 0 |a DEXAMETHASONE 
690 1 0 |a ESTRADIOL 
690 1 0 |a ESTRADIOL RECEPTOR 
690 1 0 |a GLUCOCORTICOID RECEPTOR 
690 1 0 |a ORNITHINE DECARBOXYLASE 
690 1 0 |a RADIOLIGAND 
690 1 0 |a ADRENALECTOMY 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a BINDING SITE 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a ENZYME INDUCTION 
690 1 0 |a FEMALE 
690 1 0 |a NONHUMAN 
690 1 0 |a OVARIECTOMY 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a RAT 
690 1 0 |a SPINAL CORD 
690 1 0 |a SPINAL CORD DORSAL HORN 
690 1 0 |a SPINAL CORD VENTRAL HORN 
690 1 0 |a SUBCUTANEOUS DRUG ADMINISTRATION 
690 1 0 |a ADRENALECTOMY 
690 1 0 |a ANALYSIS OF VARIANCE 
690 1 0 |a ANIMAL 
690 1 0 |a ENZYME INDUCTION 
690 1 0 |a ESTRADIOL 
690 1 0 |a FEMALE 
690 1 0 |a GLUCOCORTICOIDS 
690 1 0 |a ORNITHINE DECARBOXYLASE 
690 1 0 |a OVARIECTOMY 
690 1 0 |a RATS 
690 1 0 |a RATS, SPRAGUE-DAWLEY 
690 1 0 |a RECEPTORS, GLUCOCORTICOID 
690 1 0 |a SPINAL CORD 
690 1 0 |a SUPPORT, NON-U.S. GOV'T 
690 1 0 |a SUPPORT, U.S. GOV'T, P.H.S. 
690 1 0 |a ANIMALIA 
700 1 |a González, S. 
700 1 |a De Nicola, A.F. 
773 0 |d 1993  |g v. 52  |h pp. 677-685  |k n. 7  |p Life Sci.  |x 00243205  |w (AR-BaUEN)CENRE-749  |t Life Sciences 
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