Neurotensin inhibits neuronal Na+, K+-ATPase activity through high affinity peptide receptor

Ordieres, Marı́a Graciela López; Arnaiz, Georgina Rodrı́guez de Lores

doi:10.1016/s0196-9781(00)00183-2

Cited by 29 publications

(19 citation statements)

References 34 publications

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“…-ATPase activity whereas it fails to alter Mg 2? -ATPase activity [15]. Similar findings were presented herein in synaptosomal membranes isolated from cerebral cortex of Sprague-Dawley rats early administered with saline solution.…”

Section: Discussionsupporting

confidence: 89%

“…-ATPase activity of cerebral cortex synaptosomal membranes. This effect is entirely prevented by SR 48692, antagonist for high affinity neurotensin receptor (NTS1) [15]. Present results showed that inhibition of NO synthesis by postnatal administration of L-NAME to rats prevented further inhibition of synaptosomal membrane Na ?…”

Section: Discussionmentioning

confidence: 56%

“…-ATPase activity, to observe that the peptide inhibits the enzyme present in cortical synaptosomal membranes. This effect is entirely prevented by the presence of NTS1 receptor antagonist SR 48692 or pretreatment with dopaminergic D2 antagonist haloperidol [15,16].…”

Section: Introductionmentioning

confidence: 97%

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Postnatal Nitric Oxide Inhibition Modifies Neurotensin Effect on ATPase Activity

et al. 2011

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We have previously showed that peptide neurotensin inhibits neuronal Na(+), K(+)-ATPase activity, an effect which involves high affinity neurotensin receptor. Nitric oxide (NO) acts as a neurotransmitter or as a neuromodulator when it is synthesized by neuronal nitric oxide synthase. Neurotensin effect on Na(+), K(+)-ATPase activity was evaluated in cortical synaptosomal membranes isolated from rats injected at 3, 4 and 5 postnatal days with saline (control) or N (ω)-nitro-L-arginine methyl esther (L-NAME), a nitric oxide synthase inhibitor. Assays were carried out at two stages: juvenile (35 days) and adult (56 days) ages. In an open field task, results recorded in juvenile rats markedly differed from those obtained in adult rats. The presence of neurotensin at 3.5 × 10(-8)-3.5 × 10(-6 )M concentration decreased 16-34% Na(+), K(+)-ATPase activity in membranes purified from control animals. At variance, the peptide failed to alter this enzyme activity in membranes obtained after L-NAME treatment. After administration of L-NAME, [(3)H]-ouabain binding to membranes isolated from adult male rats decreased 64% in the presence of 1.0 × 10(-6 )M neurotensin, a peptide concentration which only slightly decreased binding to membranes isolated from juvenile rats. It is postulated that early postnatal NO dysfunction may exert a permanent change in neurotensin system that influence later Na(+), K(+)-ATPase response to neurotensin.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 56%

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Postnatal Nitric Oxide Inhibition Modifies Neurotensin Effect on ATPase Activity

et al. 2011

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“…, K ? -ATPase activity, an effect fully blocked by SR 48692, indicating the involvement of NTS1 receptor [39,40]. Na ?…”

Section: Discussionmentioning

confidence: 99%

High-affinity Neurotensin Receptor is Involved in Phosphoinositide Turnover Increase by Inhibition of Sodium Pump in Neonatal Rat Brain

et al. 2008

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Phosphoinositide (PI) metabolism is enhanced in neonatal brain by activation of neurotransmitter receptors and by inhibition of the sodium pump with ouabain or endogenous inhibitor termed endobain E. Peptide neurotensin inhibits synaptosomal membrane Na(+), K(+)-ATPase activity, an effect blocked by SR 48692, a selective antagonist for high-affinity neurotensin receptor (NTS1). The purpose of this study was to evaluate potential participation of NTS1 receptor on PI hydrolysis enhancement by sodium pump inhibition. Cerebral cortex miniprisms from neonatal Wistar rats were preloaded with [(3)H]myoinositol in buffer during 60 min and further preincubated for 0 min or 30 min in the absence or presence of SR 48692. Then, ouabain or endobain E were added and incubation proceeded during 20 or 60 min. Reaction was stopped with chloroform/methanol and [(3)H]inositol-phosphates (IPs) accumulation was quantified in the water phase. After 60-min incubation with ouabain, IPs accumulation values reached roughly 500% or 860% in comparison with basal values (100%), if the preincubation was omitted or lasted 30 min, respectively. Values were reduced 50% in the presence of SR 48692. In 20-min incubation experiments, IPs accumulation by ouabain versus basal was 300% or 410% if preincubation was 0 min or 30 min, respectively, an effect blocked 23% or 32% with SR 48692. PI hydrolysis enhancement by endobain E was similarly blocked by SR 48692, being this effect higher when sample incubation with the endogenous inhibitor lasted 60 min versus 20 min. Present results indicate that PI hydrolysis increase by sodium pump inhibition with ouabain or endobain E is partially diminished by SR 48692. It is therefore suggested that NTS1 receptor may be involved in cell signaling system mediated by PI turnover.

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“…, K ? -ATPase activity is inhibited by peptide neurotensin, an effect entirely blocked by the presence of SR 48692, antagonist of high affinity neurotensin NTS1 receptor [17,18]. Neurotensin inhibitory effect on Na ?…”

Section: Introductionmentioning

confidence: 97%

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

Ordieres

Arnaiz

2009

Neurochem Res

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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.

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Neurotensin inhibits neuronal Na+, K+-ATPase activity through high affinity peptide receptor

Cited by 29 publications

References 34 publications

Postnatal Nitric Oxide Inhibition Modifies Neurotensin Effect on ATPase Activity

Postnatal Nitric Oxide Inhibition Modifies Neurotensin Effect on ATPase Activity

High-affinity Neurotensin Receptor is Involved in Phosphoinositide Turnover Increase by Inhibition of Sodium Pump in Neonatal Rat Brain

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

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