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Current Topics in Peptide & Protein Research   Volumes    Volume 14 
High affinity receptors, and not the low affinity receptors of neurotensin are involved in neuronal Na+, K+-ATPase inhibition by the peptide
Anabel Álvarez Juliá, Alicia Gutnisky, María Graciela López Ordieres, Georgina Rodríguez de Lores Arnaiz
Pages: 27 - 32
Number of pages: 6
Current Topics in Peptide & Protein Research
Volume 14 

Copyright © 2013 Research Trends. All rights reserved

Neurotensin acts as a neuromodulator or as a neurotransmitter that binds to a group of receptors. Two of the receptors, namely NTS1 and NTS2, bind to neurotensin with high affinity and low affinity, respectively. Neurotensin added in vitro inhibits synaptosomal membrane Na+, K+-ATPase activity. This effect seems to be mediated by NTS1 receptor because it is fully blocked by antagonist SR 48692. Herein neurotensin effect was assayed after administration of SR 48692 and levocabastine which are antagonists for NTS1 and NTS2 receptors, respectively. Male Wistar rats were administered by i.p. injection, with 150 µg/kg SR 48692 (Sanofi-Aventis U.S., Inc.) suspended in the vehicle (0.01% Tween 80 in saline solution), 50 μg/kg levocabastine (disolved in saline solution) and the corresponding vehicle solutions. Thirty minutes later, the animals were sacrificed, cerebral cortices removed, separately pooled, and processed to obtain synaptosomal membranes. In membrane samples, Na+, K+- and Mg2+-ATPase activities were determined in the absence and presence of 3.5 x 10-6 M neurotensin. Basal Na+, K+-ATPase activity in membranes isolated from control rats (vehicle injected) decreased roughly by 60% by the peptide. This effect was entirely prevented by the administration of NTS1 antagonist SR 48692. Administration of levocabastine, which enhanced basal Na+, K+-ATPase activity, failed to prevent neurotensin inhibitory effect on this enzyme activity. Mg2+-ATPase activity remained unaltered in all conditions tested. It is concluded that Na+, K+-ATPase 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
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