IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
HIGH AFFINITY RECEPTORS BUT NOT LOW AFFINITY RECEPTORS FOR NEUROTENSIN ARE INVOLVED IN NEURONAL Na, K-ATPase INHIBITION BY THE PEPTIDE
Autor/es:
G. RODRÍGUEZ DE LORES ARNAIZ; A. GUTNISKY; A. ÁLVAREZ JULIÁ ; M. G. LÓPEZ ORDIERES.
Lugar:
Long Beach, California,
Reunión:
Congreso; XXXXV Congreso de la Sociedad Americana de Neuroquímica (ASN); 2014
Institución organizadora:
ASN
Resumen:
Neurotensin is a tridecapeptide which can act as a neuromodulator or as a neurotransmitter, and binds to a group of receptors. Two of them, named NTS1 and NTS2, bind neurotensin with high and low affinity, respectively. Neurotensin added in vitro inhibits synaptosomal membrane Na/K-ATPase activity. This effect seems mediated by NTS1 receptor because it is fully blocked by antagonist SR 48692 (Sanofi-Aventis, U.S., Inc.). To study further the involvement of neurotensin receptors in Na/K-ATPase  modulation by neurotensin, SR 48692 and levocabastine - respectively antagonists for NTS1 and NTS2 receptors - were used. Lots of 6 male Wistar rats were administered i.p. with 150 microg/kg SR 48692 suspended in the vehicle (0.01% Tween 80 in saline solution), 50 microg/kg levocabastine (disolved in saline solution) and the corresponding vehicle solutions. Thirty minutes later, animals were sacrificed, cerebral cortices removed, separately pooled, and processed to obtain crude and synaptosomal membrane preparations. Basal Na/K-ATPase activity in control synaptosomal membranes (vehicle injected) decreased 50% in the presence of 3.5 x 10-6M. Administration of SR 48692 entirely prevented neurotensin inhibitory effect on Na/K-ATPase activity but failed to alter basal enzyme activity. Administration of levocabastine enhanced roughly 50% both basal Na/K-ATPase activity in synaptosomal membranes and basal high affinity 3H-ouabain binding to brain membranes. This treatment failed to prevent neurotensin inhibitory effect on Na/K-ATPase activity or on high affinity 3H-ouabain binding. Results gave additional evidence that Na/K-ATPase activity inhibition by neurotensin seems mediated only by NTS1 receptor because the administration of NTS1 antagonist SR 48692, and not the NTS2 antagonist levocabastine prevented the effect of the peptide.