Specific involvement of neurotensin type 1 receptor in the neurotensin‐mediated <i>in vivo</i> dopamine efflux using knock‐out mice

Leonetti, M.; Brun, P; Clerget, Magali; Steinberg, R.; Soubrié, Philippe; Renaud, Bernard; Suaud-Chagny, Marie-Françoise

doi:10.1046/j.1471-4159.2003.02231.x

Cited by 27 publications

(19 citation statements)

References 29 publications

(45 reference statements)

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“…The persistent action of quinpirole on NMDA receptor-mediated currents is in agreement with the action of quinpirole in the hippocampus and prefrontal cortex (Beazely et al, 2006;Kotecha et al, 2002). Because NT-induced DA release is dramatically reduced in Ntsr1-KO mice (Leonetti et al, 2004), it is unlikely that DA release from DA/NTergic fibers is increased in Ntsr1-KO mice. Rather, we speculate that the mechanism 1 is based on the absence of inhibitory constraint by Ntsr1 on D 2 -like receptors.…”

Section: Ntsr1 Regulates Amygdala Ltpsupporting

confidence: 75%

Heightened Amygdala Long-Term Potentiation in Neurotensin Receptor Type-1 Knockout Mice

Amano

Wada

Yamada

et al. 2008

Neuropsychopharmacol

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Neurotensin receptor type-1 (Ntsr1) is the main receptor subtype that underlies neurotensin (NT)-mediated modulation of the dopamine (DA) system. Although NT and DA coexist in the basolateral nucleus of the amygdala (BLA), the function of Ntsr1 in the amygdala is not well characterized. In the present study, we utilized Ntsr1 knockout (Ntsr1-KO) mice to examine the role of Ntsr1 in the amygdala. In acute brain slices of Ntsr1-KO mice, synaptic currents elicited in BLA pyramidal neurons by electrical stimulation of the lateral nucleus of the amygdala (LA) were greatly potentiated by tetanic stimulation (BLA-long-term potentiation (LTP)). Such potentiation was not evident in pyramidal neurons of wild-type mice. In the presence of an antagonist of Ntsr1, SR48692, BLA-LTP was consistently observed in the neurons of wild-type mice, suggesting that both inherited deletion and acute pharmacological blockade of Ntsr1 induce BLA-LTP. BLA-LTP in Ntsr1-KO mice was impaired by sulpiride, a DA D 2 -like receptor antagonist. Conversely, quinpirole, a D 2 -like receptor agonist, induced pronounced BLA-LTP in wild-type mice, suggesting the upregulation of D 2 -like receptor activity in Ntsr1-KO mice. The ratio of NMDA receptor-mediated to non-NMDA receptor-mediated synaptic currents in Ntsr1-KO mouse BLA neurons was approximately double that measured in wild-type mouse neurons. Furthermore, quinpirole potentiated NMDA receptormediated synaptic currents in the BLA of wild-type mice. These results suggest that, without Ntsr1, synaptic responses from the LA to BLA pyramidal neurons undergo LTP in response to tetanus stimulation through facilitation of D 2 -like receptor-induced activation of NMDA receptors.

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Section: Ntsr1 Regulates Amygdala Ltpsupporting

confidence: 75%

Heightened Amygdala Long-Term Potentiation in Neurotensin Receptor Type-1 Knockout Mice

Amano

Wada

Yamada

et al. 2008

Neuropsychopharmacol

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“…NTS1 is localized both pre- and post-synaptically with DA D 2 receptors (Delle Donne et al, 2004) in the striatum, ventral midbrain, and nucleus accumbens. Its activation stimulates Ca ++ release (Beauregard et al, 1992) and modulates DA transmission (Gully et al, 1993; Leonetti et al, 2004). Additionally, the lack of NT causes altered responses to antipsychotic drugs in mice (Dobner et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Hyperactivity of the dopaminergic system in NTS1 and NTS2 null mice

Liang

Boules

et al. 2010

Neuropharmacology

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Neurotensin (NT) is a tridecapeptide that acts as a neuromodulator in the central nervous system mainly through two NT receptors, NTS1 and NTS2. The functional-anatomical interactions between NT, the mesotelencephalic dopamine system, and structures targeted by dopaminergic projections have been studied. The present study was conducted to determine the effects of NT receptor subtypes on dopaminergic function with the use of mice lacking either NTS1 (NTS1−/−) or NTS2 (NTS2−/−). Basal and amphetamine-stimulated locomotor activity was determined. In vivo microdialysis in freely moving mice, coupled with HPLC-ECD, was used to detect basal and d-amphetamine-stimulated striatal extracellular dopamine levels. In vitro radioligand binding and synaptosomal uptake assays for the dopamine transporters were conducted to test for the expression and function of the striatal pre-synaptic dopamine transporter. NTS1−/− and NTS2−/− mice had higher baseline locomotor activity and higher basal extracellular dopamine levels in striatum. NTS1−/− mice showed higher locomotor activity and exaggerated dopamine release in response to d-amphetamine. Both NTS1−/− and NTS2−/− mice exhibited lower dopamine D1 receptor mRNA expression in the striatum relative to wild type mice. Dopamine transporter binding and dopamine reuptake in striatum were not altered. Therefore, lack of either NTS1 or NTS2 alters the dopaminergic system. The possibility that the dysregulation of dopamine transmission might stem from a deficiency in glutamate neurotransmission is discussed. The data strengthen the hypothesis that NT receptors are involved in the pathogenesis of schizophrenia and provide a potential model for the biochemical changes of the disease.

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“…There is a very high coincidence of expression of NT in dopaminergic cells, and there are significant modulatory interactions between the NT and dopamine systems (Nemeroff, 1986;Binder et al, 2001;Leonetti et al, 2004;Roubert et al, 2004). NT appears to impact other neurotransmitter circuits that are innervated by the dopamine system.…”

Section: Introductionmentioning

confidence: 99%

Genetic Analysis of the Hypothalamic Neurotensin System

Garlow

Boone

Kinkead

et al. 2005

Neuropsychopharmacol

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This study used B Â D recombinant inbred mice to detect and localize genes that control the hypothalamic neurotensin (NT) system. Abundance of transcripts that encode NT and NT receptors 1, 2, and 3 (NTR1, NTR2, and NTR3) in total hypothalamic RNA was the quantitative trait measured. Analysis of transcript abundance data revealed associations with quantitative trait loci (QTL) for NT transcript abundance (NTta) on chromosome 1, 3, 6, 7, 8, and 9; for NTR1ta on chromosome 3, 8, 12, and X; for NTR2ta on chromosome 2, 4, 9, 10, 12, 13, and 17; for NTR3ta on chromosome 1, 7, 11, and 12. NTta QTL on chromosomes 3, 7, and 8 coincide with QTL previously identified that impact NT peptide content and NTR2ta QTL on chromosome 2 and 12 coincide with genes previously associated with NTR2 receptor abundance. The NTta, NTR1ta, and NTR3ta QTL were not linked to their respective structural genes, but there is a highly significant (po0.001) association for NTR2ta on chromosome 12 that includes the Ntsr2 structural gene. There are areas of potential shared genetic regulation between NTta and NTR3ta on chromosome 1 and 7 and for all three receptors on proximal chromosome 12. The NTta QTL on chromosome 9 includes the dopamine D2 receptor (Drd2) gene and QTL involved in responses to dopaminergic agents (Hts), antipsychotics (Hpic1) and cocaine (Cocrb8), and ethanol (Etohc3). These results further strengthen the hypothesis that the NT system is involved in mediating the actions of antipsychotic agents and drugs of abuse.

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Specific involvement of neurotensin type 1 receptor in the neurotensin‐mediated in vivo dopamine efflux using knock‐out mice

Cited by 27 publications

References 29 publications

Heightened Amygdala Long-Term Potentiation in Neurotensin Receptor Type-1 Knockout Mice

Heightened Amygdala Long-Term Potentiation in Neurotensin Receptor Type-1 Knockout Mice

Hyperactivity of the dopaminergic system in NTS1 and NTS2 null mice

Genetic Analysis of the Hypothalamic Neurotensin System

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