Activation of central neurotensin receptors reinstates cocaine seeking in the rat: modulation by a D1/D5, but not D2/D3, receptor antagonist

Lopak, Vanessa; Erb, Suzanne

doi:10.1007/s00213-005-0089-1

Cited by 16 publications

(5 citation statements)

References 33 publications

(37 reference statements)

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“…When administered directly into the accumbens, the dopamine D1 receptor antagonist SCH-23390 has been reported to prevent cocaine-induced reinstatement of cocaine seeking, while intra-accumbens administration of the D1 receptor agonist SKF-81297 induced reinstatement of cocaine seeking (Alleweireldt et al 2003;Bachtell et al 2005). Furthermore, it appears that this role of nucleus accumbens dopamine is not specific to direct dopaminergic agonists, as SCH-23390 also impaired the ability of caffeine and neurotensin to induce cocaine-seeking behaviour (Green and Schenk 2002;Lopak and Erb 2005). From a purely pharmacological perspective, D3 receptor antagonists have been reported to reduce nicotine-induced reinstatement of nicotine seeking (Andreoli et al 2003).…”

Section: Discussionmentioning

confidence: 99%

The α4β2 nicotinic acetylcholine-receptor partial agonist varenicline inhibits both nicotine self-administration following repeated dosing and reinstatement of nicotine seeking in rats

et al. 2009

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Section: Discussionmentioning

confidence: 99%

The α4β2 nicotinic acetylcholine-receptor partial agonist varenicline inhibits both nicotine self-administration following repeated dosing and reinstatement of nicotine seeking in rats

et al. 2009

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“…Although the functional relevance of this basal ganglia NT change caused by MPD is not known, it has been demonstrated that NT pathways influence the effects of other psychostimulants. For example, NT contributes to the following effects of COC: sensitization (Rompre and Bauco 2006); reinstatement of COC‐seeking behavioral (Lopak and Erb 2005); brain stimulation reward (Rompre et al. 1992); conditioned place preference (Glimcher et al.…”

Section: Discussionmentioning

confidence: 99%

Methylphenidate alters basal ganglia neurotensin systems through dopaminergic mechanisms: a comparison with cocaine treatment

Alburges

Hoonakker

Horner

et al. 2011

Journal of Neurochemistry

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J. Neurochem. (2011) 117, 470–478. Abstract Methylphenidate (MPD) is a psychostimulant widely used to treat behavioral problems such as attention deficit hyperactivity disorder. MPD competitively inhibits the dopamine (DA) transporter. Previous studies demonstrated that stimulants of abuse, such as cocaine (COC) and methamphetamine differentially alter rat brain neurotensin (NT) systems through DA mechanisms. As NT is a neuropeptide primarily associated with the regulation of the nigrostriatal and mesolimbic DA systems, the effect of MPD on NT‐like immunoreactivity (NTLI) content in several basal ganglia regions was assessed. MPD, at doses of 2.0 or 10.0 mg/kg, s.c., significantly increased the NTLI contents in dorsal striatum, substantia nigra and globus pallidus; similar increases in NTLI were observed in these areas after administration of COC (30.0 mg/kg, i.p.). No changes in NTLI occurred within the nucleus accumbens, frontal cortex and ventral tegmental area following MPD treatment. In addition, the NTLI changes in basal ganglia regions induced by MPD were prevented when D1 (SCH 23390) or D2 (eticlopride) receptor antagonists were coadministered with MPD. MPD treatment also increased dynorphin (DYN) levels in basal ganglia structures. These findings provide evidence that basal ganglia, but not limbic, NT systems are significantly affected by MPD through D1 and D2 receptor mechanisms, and these NTLI changes are similar, but not identical to those which occurred with COC administration. In addition, the MPD effects on NT systems are mechanistically distinct from the effects of methamphetamine.

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“…While the functional relevance of these neurotensin changes caused by nicotine are not known, it has been demonstrated that neurotensin pathways influence the effects of others psychostimulants, thus, it contributes to cocaine sensitization (Rompré and Bauco, 2006), reinstatement of cocaine seeking (Lopak and Erb, 2005), and the hyperactivity caused by cocaine and amphetamine (Boules et al, 2007). Although the role for neurotensin systems in mediating the effects of cocaine and amphetamines has been extensively investigated, a role for neurotensin in nicotine effects is little studied.…”

Section: Discussionmentioning

confidence: 99%

Nicotinic and dopamine D2 receptors mediate nicotine-induced changes in ventral tegmental area neurotensin system

Alburges

Hoonakker

Hanson

2007

European Journal of Pharmacology

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Neuropeptides have been implicated in the psychopathology of stimulants of abuse. Neurotensin is a neuropeptide associated with the regulation of the nigrostriatal and mesolimbic dopamine pathways. In addition, the ventral tegmental area, a midbrain region implicated in the rewarding effects of most, if not all, addictive drugs, appears to be a particularly critical target for nicotine action. Because neurotensin has been linked with both mesolimbic and mesocortical dopamine function, we examined the impact of nicotine treatment on central nervous neurotensin systems by measuring changes in neurotensin tissue content because it has been shown that such changes reflect alterations in release and activity of this peptide system. Male Sprague-Dawley rats received multiple administrations of (+/-) nicotine 4.0 mg/kg/day (0.8 mg/kg, i.p.; 5 x 2-h intervals) in the presence or absence of selective dopamine receptor antagonists (dopamine D(1); SCH 23390 or dopamine D(2); eticlopride) or two doses of the non-selective nicotinic acetylcholine receptor antagonist (mecamylamine; 3.0 and 6.0 mg/kg, s.c.). The nicotine treatment significantly decreased neurotensin-like immunoreactivity content in the ventral tegmental area, as well as related regions such as prefrontal cortex, substantia nigra, and anterior striatal region 12-18 h after drug treatment, but not the nucleus accumbens. The nicotine-mediated decrease in the neurotensin-like immunoreactivity of the ventral tegmental area was selectively blocked by a specific dopamine D(2), but not a dopamine D(1), receptor antagonist, while mecamylamine attenuated at the low (3.0 mg/kg) and completely blocked at high (6.0 mg/kg) dose this nicotine effect. These findings with previous studies, suggest that nicotine-mediated dopamine release activates D(2) receptors which in turn increases neurotensin release, turnover and acutely reduces tissue levels in the ventral tegmental area and other limbic and basal ganglia structures.

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Activation of central neurotensin receptors reinstates cocaine seeking in the rat: modulation by a D1/D5, but not D2/D3, receptor antagonist

Abstract: The findings suggest that an interaction between NT and DA may contribute to the neurobiology of reinstatement in animals with a history of cocaine self-administration.

Cited by 16 publications

References 33 publications

The α4β2 nicotinic acetylcholine-receptor partial agonist varenicline inhibits both nicotine self-administration following repeated dosing and reinstatement of nicotine seeking in rats

The α4β2 nicotinic acetylcholine-receptor partial agonist varenicline inhibits both nicotine self-administration following repeated dosing and reinstatement of nicotine seeking in rats

Methylphenidate alters basal ganglia neurotensin systems through dopaminergic mechanisms: a comparison with cocaine treatment

Nicotinic and dopamine D2 receptors mediate nicotine-induced changes in ventral tegmental area neurotensin system

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