IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
SODIUM-POTASSIUM ATPASE CHANGES AFTER ADMINISTRATION OF LEVOCABASTINE, AN ANTAGONIST FOR NTS2 NEUROTENSIN RECEPTOR
Autor/es:
RODRÍGUEZ ; A. GUTNISKY ; M. G. LóPEZ ORDIERES
Lugar:
Atlanta
Reunión:
Congreso; XXXXVI Congreso de la Sociedad Americana de Neuroquímica (ASN); 2015
Institución organizadora:
Sociedad Americana de Neuroquímica (ASN)
Resumen:
Neurotensin behaves as a neuromodulator or as a neurotransmitter interacting with NTS1 and NTS2 receptors. Synaptosomal membrane Na+, K+-ATPase activity is inhibited in vitro by neurotensin. This effect is prevented by administration of SR 48692 (antagonist for NTS1 receptor). The administration of levocabastine (antagonist for NTS2 receptor) does not prevent Na+, K+-ATPase inhibition by neurotensin when the enzyme is assayed with ATP as substrate. Herein levocabastine was administered to rats and Na+, K+-ATPase K+ site was evaluated on assaying K+-p-nitrophenylphosphatase (K+-p-NPPase) activity in synaptosomal membranes and [3H]-ouabain binding to cerebral cortex membranes. Male Wistar rats were administered with levocabastine (50 ìg/kg, i.p., 30 min) or the vehicle (saline solution). Synaptosomal membranes were obtained from cerebral cortex by differential and gradient centrifugation. Assays were carried out in the absence (basal) and in the presence of 1.0 x 10-5M neurotensin. The activity of K+-p-NPPase was determined in media containing or not NaCl plus ATP. In such phosphorylating condition enzyme behaviour resembles that observed when ATP hydrolyses is recorded. In the absence of NaCl plus ATP, K+-p-NPPase activity was similar for levocabastine or vehicle injected (roughly 11 mmole hydrolyzed substrate per mg protein per hour). Such values remained unaltered by the presence of 1.0 x 10-5M neurotensin. In the phosphorylating medium, neurotensin decreased (80%) the enzyme activity in membranes obtained from rats injected with the vehicle but failed to alter those obtained from rats injected with levocabastine. Levocabastine administration enhanced (50%) basal [3H]-ouabain binding to cerebral cortex membranes but failed to modify neurotensin inhibitory effect on this ligand binding. It is concluded that NTS2 receptor blockade modifies the properties of neuronal Na+, K+-ATPase and that neurotensin effect on Na+, K+-ATPase involves NTS1 receptor and -at least partially- NTS2 receptor.