Clozapine Administration Modifies Neurotensin Effect on Synaptosomal Membrane Na+, K+ -ATPase Activity

Abstract

Na+, K+-ATPase is inhibited by neurotensin, an effect which involves the peptide high affinity receptor (NTS1). Neurotensin effect on cerebral cortex synaptosomal membrane Na+, K+-ATPase activity of rats injected i.p. with antipsychotic clozapine was studied. Whereas 3.5 x 10(-6) M neurotensin decreased 44% Na+, K+-ATPase activity in the controls, the peptide failed to modify enzyme activity 30 min after a single 3.0, 10.0 and 30.0 mg/kg clozapine dose. Neurotensin decreased Na+, K+-ATPase activity 40 or 20% 18 h after 3.0 or 5.6 mg/kg clozapine administration, respectively, and lacked inhibitory effect 18 h after 17.8 and 30.0 mg/kg clozapine doses. Results indicated that the clozapine treatment differentially modifies the further effect of neurotensin on synaptosomal membrane Na+, K+-ATPase activity according to time and dose conditions employed. Taken into account that clozapine blocks the dopaminergic D2 receptor, findings obtained favor the view of an interplay among neurotensinergic receptor, dopaminergic D2 receptor and Na+, K+-ATPase at synaptic membranes.

Effect of liraglutide on neural and peripheral markers of metabolic function during antipsychotic treatment in rats

“…The sodium pump (NaKATPase) is a major energy consumer, with reduced activity in adipose tissue of obese patients (Iannello et al, 2007) and in the liver and kidney of obese mice (Iannello et al, 2007; Yukimura and Bray, 1978). Few studies have examined the effects of APDs or GLP-1R agonists on NaKATPase activity (López Ordieres and Rodríguez de Lores Arnaiz, 2009; Sancar-Bas et al, 2015; Seibt et al, 2012). For example, exenatide pretreatment decreased mitochondrial abnormalities and oxidative stress while enhancing ATP synthesis and NaKATPase activity in a cell model of ischaemia (Chang et al, 2018).…”