Interaction between neuropeptide FF and opioids in the ventral tegmental area in the behavioral response to novelty

Cador, Martine; Marco, N.; Stinus, L.; Simonnet, Guy

doi:10.1016/s0306-4522(01)00587-5

Cited by 28 publications

(13 citation statements)

References 59 publications

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“…For example, infusion of the antiopioid peptide, neuropeptide FF, into the VTA reduced locomotor response to novelty, whereas an inhibitor of enkephalin degradation strongly increased novelty-induced locomotion (Cador et al, 2002). Moreover, it has been shown that chronic cocaine treatment increases m-opioid receptor density in dopaminergic projection regions both in rats (Hammer, 1989;Unterwald et al, 1992) and human cocaine addicts (Zubieta et al, 1996), indicating that dopaminergic and opioid systems have reciprocal interaction with regard to their reinforcing effects.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Effects of Repeated Social Defeat Stress on mRNA Expression and Function of μ-Opioid Receptors in the Ventral Tegmental Area of Rats

Nikulina

Miczek

Hammer

2005

Neuropsychopharmacol

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Social defeat stress alters the activity of mesocorticolimbic dopamine projections from the ventral tegmental area (VTA), a process that has been implicated in the development of sensitization and drug-seeking behavior. We showed previously that acute brief social defeat stress increased short-term expression of m-opioid receptor mRNA in the VTA. The present study assessed the presence and functional significance of m-opioid receptor mRNA expression 1 week after the last episode of social defeat stress. Social defeat stress was induced in intruder rats during short confrontations with an aggressive resident rat, and subsequent exposures behind a protective screen once a day for 5 days. Regional m-receptor mRNA levels were assessed by in situ hybridization histochemistry, and the amount of mRNA labeling was measured in the VTA and the substantia nigra (SN). Expression of m-opioid receptor mRNA was significantly higher in defeated rats relative to handled control animals in the VTA, but not in the SN. In an additional group of rats, bilateral local intra-VTA injection of the selective m-opioid receptor agonist DAMGO (1.0 mg per side) was performed 7-10 days after the last defeat stress or handling control procedure. Baseline motor activity did not differ between control and stressed rats. Intra-VTA DAMGO significantly increased locomotor activity in stressed rats compared to handled control rats. These results suggest that repeated social stress upregulates VTA m-opioid receptors and can produce locomotor activation via stimulation of these receptors. This locomotor effect is probably the consequence of enhanced disinhibition of mesolimbic dopamine neurons.

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Section: Discussionmentioning

confidence: 99%

Prolonged Effects of Repeated Social Defeat Stress on mRNA Expression and Function of μ-Opioid Receptors in the Ventral Tegmental Area of Rats

Nikulina

Miczek

Hammer

2005

Neuropsychopharmacol

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“…For feeding experiments, drug concentrations for met-enkephalin (0.025, 0.25, 2.5 nmoles/NAcc) and the enkephalin analogue DALA (0.025, 0.25, 2.5, 12.5 nmoles/NAcc) were chosen to bracket a dose of DAMGO that elicits robust feeding (0.25 nanomoles/NAcc). Thiorphan doses (4, 13, 40 nmoles/NAcc) were guided by previous reports that concentrations as low as 1–10 nmoles were sufficient to elicit significant behavioral effects (Kalivas and Richardson-Carlson, 1986, Cador et al, 2002). Finally, the DPDPE dose (4 nmoles/NAcc) was chosen to match the concentration identified in a previous report as the dose maximally effective in eliciting food intake when infused into the NAcc (Bakshi and Kelley, 1993a).…”

Section: Methodsmentioning

confidence: 99%

Modulation of feeding and locomotion through mu and delta opioid receptor signaling in the nucleus accumbens

Katsuura

Taha

2010

Neuropeptides

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Opioid signaling has been strongly implicated in driving palatable food consumption. The nucleus accumbens (NAcc) is one important site of this effect; hyperphagia elicited by administration of exogenous mu opioid receptor (MOR) ligands in this brain region has been well documented. However, the role that endogenous opioid ligands in the NAcc play in controlling food intake remains poorly understood. Enkephalins, which signal through both the MOR and delta opioid receptor (DOR), are highly expressed within a subset of NAcc neurons, and have been shown to be sensitive to manipulations of diet and motivation. To investigate a potential role for these signaling molecules in regulating palatability-driven consumption, we measured high fat chow intake in rats following a series of pharmacological manipulations of NAcc opioid signaling. NAcc infusion of the MOR agonist [D-Ala2, N-MePHe4, Gly-ol]-enkephalin (DAMGO) robustly increased palatable food intake, as has previously been demonstrated. In contrast, neither infusion of met-enkephalin, its synthetic analogue [D-ala2] Met-enkephalin (DALA) nor the DOR-specific ligand [D-Pen2, Pen5]-enkephalin (DPDPE) had significant effects on food intake. However, when administered in combination with DAMGO, DPDPE significantly suppressed the magnitude of DAMGO-evoked feeding. Further analysis of DPDPE effects revealed that the drug strongly increased locomotor activity. Suppressive effects on feeding, then, may have occurred through competition between feeding and locomotion for behavioral expression.

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“…There is evidence that a novel or surprising stimulus can evoke unconditioned responses through the release of endogenous opioids, including analgesia, and that the reduction in these responses across exposures to the stimulus is blocked by naloxone (eg, Cador et al, 2002;Foo and Westbrook, 1991;Hernandez and Watson, 1997;Izquierdo et al, 1984;Rochford and Dawes, 1993). Accordingly, naloxone disrupted the error signal, which normally drives the formation of the inhibitory association in latent inhibition.…”

Section: Discussionmentioning

confidence: 99%

Error Correction in Latent Inhibition and its Disruption by Opioid Receptor Blockade with Naloxone

Leung

Killcross

Westbrook

2013

Neuropsychopharmacol

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Latent inhibition refers to the retardation in the development of conditioned responding when a pre-exposed stimulus is used to signal an unconditioned stimulus. This effect is described by error-correction models as an attentional deficit and is commonly used as an animal model of schizophrenia. A series of experiments studied the role of error-correction mechanism in latent inhibition and its interaction with the endogenous opioid system. Systemic administration of the competitive opioid receptor antagonist naloxone before rats were pre-exposed to a target stimulus prevented latent inhibition of its subsequent fear conditioning; it was without effect on a non-preexposed stimulus and did not produce state-dependent learning (Experiments 1a and 1b). Naloxone did not reverse the latent inhibitory effect already accrued to a pre-exposed target. However, it did prevent the enhancement of latent inhibition by a long retention interval interpolated between its initial exposure and re-exposure (Experiment 2) or by a novel stimulus compounded with the pre-exposed target during re-exposure (Experiment 3). These results provide evidence that attentional loss in latent inhibition is instructed by an opioid-mediated error signal which diminishes with repeated stimulus exposures but recovers with the passage of time or reintroduction of novelty.

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Interaction between neuropeptide FF and opioids in the ventral tegmental area in the behavioral response to novelty

Cited by 28 publications

References 59 publications

Prolonged Effects of Repeated Social Defeat Stress on mRNA Expression and Function of μ-Opioid Receptors in the Ventral Tegmental Area of Rats

Prolonged Effects of Repeated Social Defeat Stress on mRNA Expression and Function of μ-Opioid Receptors in the Ventral Tegmental Area of Rats

Modulation of feeding and locomotion through mu and delta opioid receptor signaling in the nucleus accumbens

Error Correction in Latent Inhibition and its Disruption by Opioid Receptor Blockade with Naloxone

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