NO donor SIN-I potentiates monosynaptic reflexes in the cat spinal cord


Por: Manjarrez E., Rocha T., Rojas-Piloni G., Méndez I., Vélez D., Flores A.

Publicada: 1 ene 2001
Resumen:
The effect produced by the nitric oxide donor SIN-I on monosynaptic reflexes was examined. Experiments were performed on anesthetized, paralyzed and spinalized cats. Lumbar monosynaptic reflexes were produced by stimulation of Ia afferents. I.v. application of SIN-I (500 ?g/kg) produced a mean marked potentiation of 704% of pre-drug control (100%) in the amplitude of monosynaptic reflexes. In addition, in other experiments a concentration-dependent effect on the amplitude of monosynaptic reflexes was observed after microinjections of SIN-I into the ventral horn (1 ?l; 10-12-10-3 M), with a mean facilitatory effect of 355%. In both cases, the potentiation was reversible 45 min after i.v. or local application of SIN-I. These results provide the first evidence that monosynaptic reflexes can be potentiated by nitric oxide. © 2001 Lippincott Williams & Wilkins.

Filiaciones:
Manjarrez E.:
 Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, Col. San Manuel, Apartado Postal 406, Puebla, Pue. CP 72570, Mexico

Rocha T.:
 Facultad de Medicina, Benemérita Universidad Autónoma de Puebla, Col. San Manuel, Apartado Postal 406, Puebla, Pue. CP 72570, Mexico

Rojas-Piloni G.:
 Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, Col. San Manuel, Apartado Postal 406, Puebla, Pue. CP 72570, Mexico

Méndez I.:
 Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, Col. San Manuel, Apartado Postal 406, Puebla, Pue. CP 72570, Mexico

Vélez D.:
 Facultad de Medicina, Benemérita Universidad Autónoma de Puebla, Col. San Manuel, Apartado Postal 406, Puebla, Pue. CP 72570, Mexico

Flores A.:
 Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, Col. San Manuel, Apartado Postal 406, Puebla, Pue. CP 72570, Mexico
ISSN: 09594965
Editorial
Lippincott Williams and Wilkins, 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 12 Número: 12
Páginas: 2667-2671
WOS Id: 000170600500016
ID de PubMed: 11522945