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1.
Exp Neurol ; 186(2): 124-33, 2004 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-15026251

RESUMEN

The optic nerve is a CNS pathway containing molecules capable of inhibiting axon elongation. The growth program in embryonic retinal ganglion cell (RGC) neurons enables axons to regenerate in the optic nerve through at least two mechanisms. Namely, high cyclic AMP (cAMP) levels abrogate the ability of CNS molecules to inhibit elongation, and the pattern of gene expression enables axons to undergo rapid, sustained, and lengthy elongation. In adult mammals, recovery of visual function after optic nerve injury is limited by both the death of most RGC neurons and the inability of surviving axons to regenerate. We now report that a single intraocular injection of the membrane-permeable cAMP analogue dibutyryl cAMP (db cAMP) promotes the regeneration of RGC axons in the optic nerves of adult rats, but does not prevent the death of RGC neurons. This regeneration in optic nerves crushed within the orbit (2 mm from the eye) was equally effective either 1 day before or 1 day after db cAMP injection. The number of regenerating axons, which was maximal 14 days after crush, declined with increasing time after injury (i.e., 28, 56, and 112 days) and distance beyond the crush site (i.e., 0.25, 0.5, and 1.0 mm). Thus, db cAMP promotes optic nerve regeneration without increasing the survival of axotomized RGC neurons. Furthermore, since db cAMP does not enable axons to undergo rapid, sustained, and lengthy elongation, strategies that increase survival and promote these changes in elongation may critically complement the ability of db cAMP to promote regeneration.


Asunto(s)
Axones/efectos de los fármacos , Bucladesina/farmacología , Regeneración Nerviosa/efectos de los fármacos , Nervio Óptico/efectos de los fármacos , Animales , Recuento de Células/métodos , Supervivencia Celular/efectos de los fármacos , Toxina del Cólera/metabolismo , Relación Dosis-Respuesta a Droga , Femenino , Colorantes Fluorescentes/metabolismo , Peroxidasa de Rábano Silvestre/metabolismo , Compresión Nerviosa/métodos , Nervio Óptico/citología , Órbita/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Células Ganglionares de la Retina/metabolismo , Estilbamidinas/metabolismo , Factores de Tiempo
2.
J Neurol Sci ; 217(2): 131-3, 2004 Feb 15.
Artículo en Inglés | MEDLINE | ID: mdl-14706214

RESUMEN

Fifty percent of ocular myasthenia gravis (OMG) patients will progress to generalized myasthenia, 90% within 3 years from the onset of ocular symptoms. This study was performed to determine whether treatment with oral prednisone initiated and completed within 2 years from the onset of ocular symptoms would affect the progression of ocular myasthenia to generalized myasthenia gravis (GMG). Fifty-six patients were included in this review, with 27 patients in the prednisone-treated group and 29 patients in the untreated group. The treated group was initiated on 60 mg of prednisone daily with a slow taper over 3-6 months. At 2 years, significantly fewer patients in the treated group (3 of 27) progressed to generalized myasthenia when compared to the untreated group (10 of 29) (chi(2), p=0.04). Our results suggest that the early use of steroids may decrease progression of ocular to generalized myasthenia gravis. The decision to use steroids should be considered early in the course of patients diagnosed with ocular myasthenia gravis. This study should be considered preliminary and a prospective trial is warranted to confirm our observations.


Asunto(s)
Inmunosupresores/uso terapéutico , Miastenia Gravis/tratamiento farmacológico , Miastenia Gravis/prevención & control , Prednisona/uso terapéutico , Inhibidores de la Colinesterasa/uso terapéutico , Progresión de la Enfermedad , Relación Dosis-Respuesta a Droga , Esquema de Medicación , Femenino , Humanos , Masculino , Persona de Mediana Edad , Miastenia Gravis/fisiopatología , Músculos Oculomotores/efectos de los fármacos , Músculos Oculomotores/inmunología , Músculos Oculomotores/fisiopatología , Bromuro de Piridostigmina/uso terapéutico , Receptores Colinérgicos/efectos de los fármacos , Receptores Colinérgicos/inmunología , Estudios Retrospectivos , Resultado del Tratamiento
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