Extensive Co-localization of neurotensin with dopamine in rat meso-cortico-frontal dopaminergic neurons

Studler, Jeanne-Marie; Kitabgi, Patrick; Tramu, G.; Hervé, Denis; Głowiński, J.; Tassin, Jean‐Pol

doi:10.1016/0143-4179(88)90076-5

Cited by 147 publications

(58 citation statements)

References 31 publications

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“…The NTSR1 gene encodes a high-affinity neurotensin receptor, NTSR1. In the central nervous system, NT and NTSR1 are highly expressed in dopaminergic neurons (Brouard et al, 1992;Studler et al, 1988), which allows functional interactions between the NT and the DA systems at the cellular level (Binder et al, 2001). For example, animal studies suggested that NT enhances DA neuron firing (Jomphe et al, 2006;St-Gelais et al, 2004) and extracellular release of DA (Petkova-Kirova et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

The NTSR1 gene modulates the association between hippocampal structure and working memory performance

Jin¹,

Lei²,

Wang³

et al. 2013

NeuroImage

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The genetic and neural basis of working memory (WM) has been extensively studied. Many dopamine (DA) related genes, including the NTSR1 gene (a DA modulator gene), have been reported to be associated with WM performance. The NTSR1 protein is predominantly expressed in the cerebral cortex and the hippocampus, the latter of which is closely involved in WM processing based on both lesion and fMRI studies. Thus far, however, no study has examined the joint effects of NTSR1 gene polymorphism and hippocampal morphology on WM performance. Participants of the current study were 330 healthy Chinese college students. WM performance was measured with a 2-back WM paradigm. Structural MRI data were acquired and then analyzed using an automated procedure with atlas-based FreeSurfer segmentation software (v 4.5.0) package. Linear regression analyses were conducted with a NTSR1 C/T polymorphism which was previously reported to be associated with WM (rs4334545), hippocampal volume, and their interaction as predictors of WM performance, with gender and intracranial volume (ICV) as covariates. Results showed a significant interaction between NTSR1 genotype and hippocampal volume (p b .05 for both the left and right hippocampi). Further analysis showed that the correlation between hippocampal volume and WM scores was significant for carriers of the NTSR1 T-allele (p b .05 for both hippocampi), but not for CC homozygotes. These results indicate that the association between hippocampal structure and WM performance was modulated by variation in the NTSR1 gene, and suggest that further studies of brain-behavior associations should take genetic background information into account.

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Section: Discussionmentioning

confidence: 99%

The NTSR1 gene modulates the association between hippocampal structure and working memory performance

Jin¹,

Lei²,

Wang³

et al. 2013

NeuroImage

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“…Activation of these D 2 autoreceptors decreases DA release but increases release of the colocalized transmitter neurotensin (NT; see Bean and Roth, 1992). In the PFC, NT is localized exclusively to dopaminergic axons (Studler et al, 1988). Thus, activation of D 2 autoreceptors decreases DA release but increases NT release from mesoprefrontal cortical neurons.…”

Section: Introductionmentioning

confidence: 99%

The Neurotensin Agonist PD149163 Increases Fos Expression in the Prefrontal Cortex of the Rat

Petrie

Bubser

Casey

et al. 2004

Neuropsychopharmacol

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Dopaminergic axons innervating the prefrontal cortex (PFC) target both pyramidal cells and GABAergic interneurons. Many of these dopamine (DA) axons in the rat coexpress the peptide neurotransmitter neurotensin. Previous electrophysiological data have suggested that neurotensin activates GABAergic interneurons in the PFC. Activation of D2-like DA receptors increases extracellular GABA levels in the PFC, as opposed to the striatum, where D2 receptor activation inhibits GABAergic neurons. Because activation of presynaptic D 2 release-modulating autoreceptors in the PFC suppresses DA release but increases release of the cotransmitter neurotensin, D2 agonists may enhance the activity of GABAergic interneurons via release of neurotensin. In order to determine if neurotensin can activate GABAergic interneurons, we treated rats with the peptide neurotensin agonist, PD149163, and examined Fos expression in PFC neurons. Systemic administration of PD149163 increased overall Fos expression in the PFC, but not in the dorsal striatum. PD149163 induced Fos in PFC interneurons, as defined by the presence of calcium-binding proteins, and in pyramidal cells. Pretreatment with the high-affinity neurotensin antagonist, SR48692, blocked neurotensin agonist-induced Fos expression. These data suggest that neurotensin activates interneurons in the PFC of the rat.

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“…Likewise, several lines of evidence suggest that neurotensin (NT), a neuropeptide closely associated with DA systems, could play a role in stimulant-induced sensitization. Indeed, NT has been shown to co-exist with DA in a subset of mesencephalic neurons that project to the NAC and mPFC (Hökfelt et al 1984; Kalivas and Miller 1984;Seroogy et al 1987;Studler et al 1988; Bayer et al 1991) and to be coreleased with DA following psychostimulant administration (During et al 1992; Hertel et al 1996). Moreover, the injection of NT into the VTA produces psychostimulant-like behavioral and neurochemical activation effects such as increased locomotor activity and rearing (Kalivas et al 1983; Cador et al 1985) and enhanced extracellular levels of DA in the NAC (Kalivas and Duffy 1990;Laitinen et al 1990;Sotty et al 1998).…”

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confidence: 99%

Chronic Blockade of Neurotensin Receptors Strongly Reduces Sensitized, but Not Acute, Behavioral Response to D-amphetamine

Panayi

Dorso

Lambás‐Señas

et al. 2002

Neuropsychopharmacology

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This study investigated the effect of a chronic blockade of neurotensin (NT) receptors on the sensitized behavioral response to amphetamine using a nonpeptide NT receptor antagonist, SR 48692. Rats received four injections of D-amphetamine (0.5 or 1 mg/kg, IP) every other day (day 1, 3, 5 and 7) and were then challenged with the same dose of amphetamine after a 6-day withdrawal (day 14) to establish the presence of locomotor sensitization. Daily administration of SR 48692 (1 mg/kg, IP) throughout the amphetamine regimen (day 1 to day 14) almost completely blocked the sensitized locomotor response to amphetamine without affecting stereotyped behaviors (experiment 1). The decreased amphetamine-induced sensitization in chronically SR 48692-treated rats did not appear to result from an influence on basal locomotor activity, as chronic SR 48692 treatment did not modify the spontaneous locomotor activity developed in response to mild stresses (experiment 2). Moreover, we showed that chronic pretreatment with SR 48692 (1 mg/kg, 14 daily IP injections) had no effect on the locomotor activation induced by a single IP administration of amphetamine (experiment 3). These data suggest that a sustained blockade of NTRepeated intermittent administration of psychostimulants, such as amphetamine and cocaine, leads to a progressive enhancement of their behavioral stimulant effects, as well as a long-lasting hyperreactivity in response to environmental or pharmacological challenges (Antelman et al. 1980;Kalivas and Stewart 1991). This phenomenon, termed behavioral sensitization, is considered as a useful animal model for drug-induced psychosis and drug craving in humans (Robinson and Becker 1986;Robinson and Berridge 1993;Lieberman et al. 1997;Laruelle 2000).The mesoaccumbens dopaminergic (DA) system, which originates within the ventral tegmental area (VTA) and projects to the nucleus accumbens (NAC), plays an important role in the behavioral sensitization to psychostimulants. Thus, repeated injections of am- phetamine into the VTA produce sensitized locomotor responses to systemic injections of amphetamine, cocaine and morphine. In contrast, although amphetamine produces locomotor stimulation upon acute injection into the NAC, repeated intra-NAC injections do not lead to sensitization (Kalivas and Weber 1988;Vezina and Stewart 1990; Hooks et al. 1992; Cador et al. 1995). Other studies have established that the mechanisms leading to the induction of sensitization require the action of DA, somatodendritically released by amphetamine, on D1 receptors in the VTA whereas DA release in the NAC appears as the prime event for the expression of behavioral sensitization (Vezina 1993(Vezina , 1996Pierce and Kalivas 1997a). However, recent studies support the view that the neural underpinnings of behavioral sensitization implicate additional limbic areas and neurotransmitters such as the medial prefrontal cortex (mPFC) and its glutamatergic components (Wolf 1998; Cador et al. 1999) or the ventral pallidum and its GABAergic components (Pier...

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Extensive Co-localization of neurotensin with dopamine in rat meso-cortico-frontal dopaminergic neurons

Cited by 147 publications

References 31 publications

The NTSR1 gene modulates the association between hippocampal structure and working memory performance

The NTSR1 gene modulates the association between hippocampal structure and working memory performance

The Neurotensin Agonist PD149163 Increases Fos Expression in the Prefrontal Cortex of the Rat

Chronic Blockade of Neurotensin Receptors Strongly Reduces Sensitized, but Not Acute, Behavioral Response to D-amphetamine

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