The Effects of Naloxone on Expression and Acquisition of Ethanol Place Conditioning in Rats

Bormann, Nancy M.; Cunningham, Christopher L.

doi:10.1016/s0091-3057(97)00304-3

Cited by 36 publications

(29 citation statements)

References 38 publications

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“…These findings fit well with previously reported data showing that voluntary alcohol consumption and/or preference are decreased in CB 1 À/À mice (Hungund et al, 2002(Hungund et al, , 2003Poncelet et al, 2003;Wang et al, 2003;Naassila et al, 2004). There is a large body of experimental reports demonstrating reliable ethanolinduced CPP in inbred and outbred mice (Crabbe et al, Rewarding effects of ethanol in CB1 ko mice H Houchi et al 1992; Bormann and Cunningham, 1997). In the present study, ethanol at the dose of 0.5 g/kg produced maximal place conditioning effect in wild-type mice.…”

Section: Discussionsupporting

confidence: 90%

CB1 Receptor Knockout Mice Display Reduced Ethanol-Induced Conditioned Place Preference and Increased Striatal Dopamine D2 Receptors

Houchi

Babovic

Pierrefiche

et al. 2004

Neuropsychopharmacol

174

145

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Cannabinoids and ethanol activate the same reward pathways, and recent advances in the understanding of the neurobiological basis of alcoholism suggest that the CB 1 receptor system may play a key role in the reinforcing effects of ethanol and in modulating ethanol intake. In the present study, male CB 1 receptors knockout mice generated on a CD1 background displayed decreased ethanol-induced conditioned place preference (CPP) compared to wild-type (CB 1 þ / þ ) mice. Ethanol (0.5, 1.0, 1.5, and 2.0 g/kg) induced significant CPP in CB 1 þ / þ mice at all doses tested, whereas it induced significant CPP only at the highest dose of ethanol (2.0 g/kg) in CB 1 À/À mice.However, there was no genotypic difference in cocaine (20 mg/kg)-induced CPP. There was also no genotypic difference, neither in cocaine (10-50 mg/kg) nor in D-amphetamine (1.2-5 mg/kg)-induced locomotor effects. In addition, mutant and wild-type mice did not differ in sensitivity to the anxiolytic effects of ethanol (1.5 g/kg) when tested using the elevated plus maze. Interestingly, this decrease in ethanol efficacy to induce CPP in CB 1 À/À mice was correlated with an increase in D2/D3 receptors, as determined by [ 3 H]raclopride binding, whereas there was no difference in D1-like receptors, as determined by [ 3 H]SCH23390 binding, measured in the striatum from drug-naïve mice. This increase in D2/D3 binding sites observed in CB 1 knockout mice was associated with an altered locomotor response to the D2/D3 agonist quinpirole (low doses 0.02-0.1 mg/kg) but not to an alteration of quinpirole (0.1-1.0 mg/kg)-induced CPP compared to wild-type mice. Altogether, the present results indicate that lifelong deletion of CB 1 receptors reduced ethanol-induced CPP and that these reduced rewarding effects of ethanol are correlated to an overexpression of striatal dopamine D2 receptors.

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Section: Discussionsupporting

confidence: 90%

CB1 Receptor Knockout Mice Display Reduced Ethanol-Induced Conditioned Place Preference and Increased Striatal Dopamine D2 Receptors

Houchi

Babovic

Pierrefiche

et al. 2004

Neuropsychopharmacol

174

145

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“…There is a large body of experimental reports demonstrating reliable ethanol-induced CPP in inbred and outbred mice (Cunningham et al, 1991;Crabbe et al, 1992;Cunningham, 1995;Bormann and Cunningham, 1997). In the present study, ethanol at the dose of 0.8 g/kg produced maximal place conditioning effect in outbred NMRI mice.…”

Section: Discussionsupporting

confidence: 52%

Acquisition, Expression, and Reinstatement of Ethanol-Induced Conditioned Place Preference in Mice: Effects of Opioid Receptor-Like 1 Receptor Agonists and Naloxone

Kuzmin

Sandin²,

Terenius³

et al. 2003

J Pharmacol Exp Ther

165

135

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The ability of the two opioid receptor-like receptor 1 (ORL1) agonists nociceptin (5 nmol i.c.v.) and synthetic (1S,3aS)-8-(2,3,3a,4,5,6-hexahydro-1H-phenalen-1-yl)-1-phenyl-1,3,8-triaza-spiro[4.5]decan-4-one hydrochloride (Ro 64-6198; 0.1, 0.3, and 1.0 mg/kg i.p.) and the opioid antagonist naloxone (0.1, 1.0, and 10.0 mg/kg s.c.) to modify ethanolinduced conditioned place preference was examined in NMRI male mice. The ORL1 agonists were found to significantly reduce the acquisition, expression, and ethanolinduced reinstatement of conditioned place preference. Unlike the ORL1 agonists, naloxone at the doses relevant for opioid receptor blockade failed to significantly influence the acquisition of ethanol-induced conditioned place preference. However, naloxone at 1.0 but not 0.1 mg/kg s.c. potently blocked the expression of ethanol-induced conditioned place preference and significantly inhibited ethanol-induced reinstatement of the conditioned place preference after extinction. Separate experiments indicated that nociceptin and Ro 64-6198 are both devoid of reinforcing or aversive properties. Naloxone, however, at 1.0 and 10.0 mg/kg, produced conditioned place aversion, indicating motivational properties of its own. Both nociceptin and Ro 64-6198 reduced locomotor activity after acute administration. However, tolerance developed very quickly to this effect and already after three i.c.v. (or i.p.) injections, there was no significant reduction of locomotor activity. It is concluded that ORL1 agonists can modulate the acquisition, expression, and reinstatement of the conditioned reinforcing effects of ethanol with no reinforcing or aversive properties of their own. This property might be a potential advantage in the treatment of alcoholism compared with nonselective opioid antagonist naltrexone.Relapse to alcohol use after periods of abstinence is a common feature of alcoholism. Animal models have contributed to the identification of factors that may underlie the motivational aspects of ethanol and that contribute to relapse to ethanol taking. Drug-seeking behavior for ethanol can be initiated or maintained not only by the primary, reinforcing effects of the drugs themselves but also by secondary, drug-associated stimuli (for review, see O'Brien, 1975). The most common experimental model used to study relapse to drug seeking has been the reinstatement procedure. After training to make a response to self-administer a drug and the subsequent extinction of the acquired response, an acute noncontingent injection of test drug (or acute stress) results in the reinstatement of responding (Carroll and Comer, 1996). The conditioned place preference (CPP) procedure provides an alternative experimental approach to examine mechanisms underlying relapse. In this procedure a particular stimulus context or test environment is paired with the effects of the drug, without the animal having to learn to make an explicit response to obtain the drug. In the test trial, the animal is allowed to freely move between the test envir...

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“…If ICI 118,551 or prazosin were aversive, the temporal proximity of the drug with the preferred, drug-paired floor during the initial test via immediate posttest administration might decrease preference on a subsequent test (Bormann and Cunningham 1997). We demonstrated here that administration of ICI 118,551 or prazosin following a single CS exposure, identical to the parameters in our post-retrieval studies, had no effect on a subsequent test.…”

Section: Discussionsupporting

confidence: 45%

“…A GRID floor consists of 2.3-mm stainless steel rods mounted 13 mm apart in an acrylic frame. A HOLE floor consists of perforated black acrylic with 13-mm round holes on 19-mm staggered centers (modified from the method of Bormann and Cunningham 1997). Pilot experiments have demonstrated that rats show approximately equal preference for the two floor types.…”

Section: Apparatusmentioning

confidence: 99%

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists

Bernardi¹,

Ryabinin²,

Berger³

et al. 2009

Learn. Mem.

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Previous work has demonstrated post-retrieval impairment in associative learning paradigms, including those mediated by drugs of abuse, using nonspecific b-adrenergic receptor (b-AR) antagonists. Remarkably little is known about the role of the specific b-AR subtypes, or other adrenergic receptors, in these effects. The current study examined the effects of b 1 and b 2 , as well as a 1 -adrenergic receptor antagonism following retrieval of a cocaine conditioned place preference (CPP). We found that rats administered the b 2 antagonist ICI 118,551 (8 mg/kg intraperitoneal [IP]) or the a 1 antagonist prazosin (1 mg/kg IP) following a drug-free test for CPP showed attenuated preference during a subsequent test, while the b 1 antagonist betaxolol (5 or 10 mg/kg IP) and a lower dose of prazosin (0.3 mg/kg IP) had no effect. Furthermore, posttest microinfusion of ICI 118,551 (6 nmol/side) or prazosin (0.5 nmol/side) into the basolateral amygdala (BLA) also impaired a subsequent preference. Systemic or intra-BLA ICI 118,551 or prazosin administered to rats in their home cages, in the absence of a preference test, had no effect on CPP 24 h later. ICI 118,551 also attenuated the FOS response in the BLA induced by the CPP test. These results are the first to demonstrate a role for a 1 -and b 2 -specific adrenergic mechanisms in post-retrieval memory processes. These systemic and site-specific injections, as well as the FOS immunohistochemical analyses, implicate the importance of specific noradrenergic signaling mechanisms within the BLA in post-retrieval plasticity.

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The Effects of Naloxone on Expression and Acquisition of Ethanol Place Conditioning in Rats

Cited by 36 publications

References 38 publications

CB1 Receptor Knockout Mice Display Reduced Ethanol-Induced Conditioned Place Preference and Increased Striatal Dopamine D2 Receptors

CB1 Receptor Knockout Mice Display Reduced Ethanol-Induced Conditioned Place Preference and Increased Striatal Dopamine D2 Receptors

Acquisition, Expression, and Reinstatement of Ethanol-Induced Conditioned Place Preference in Mice: Effects of Opioid Receptor-Like 1 Receptor Agonists and Naloxone

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists

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The Effects of Naloxone on Expression and Acquisition of Ethanol Place Conditioning in Rats

Cited by 36 publications

References 38 publications

CB1 Receptor Knockout Mice Display Reduced Ethanol-Induced Conditioned Place Preference and Increased Striatal Dopamine D2 Receptors

CB1 Receptor Knockout Mice Display Reduced Ethanol-Induced Conditioned Place Preference and Increased Striatal Dopamine D2 Receptors

Acquisition, Expression, and Reinstatement of Ethanol-Induced Conditioned Place Preference in Mice: Effects of Opioid Receptor-Like 1 Receptor Agonists and Naloxone

Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β2- and α1-adrenergic antagonists

Contact Info

Product

Resources

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Post-retrieval disruption of a cocaine conditioned place preference by systemic and intrabasolateral amygdala β₂- and α₁-adrenergic antagonists