Susceptibility to conditioned place preference induced by addictive drugs in mice of the C57BL/6 and DBA/2 inbred strains

Orsini, Cristina; Bonito‐Oliva, Alessandra; Conversi, David; Cabib, Simona

doi:10.1007/s00213-005-2259-6

Cited by 102 publications

(88 citation statements)

References 34 publications

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“…For place conditioning with pharmacological stimuli, one of the patterns was consistently paired with saline and the other with cocaine (20 mg/kg i.p., CPP) or LiCl (3.0 meq/kg i.p., CPA) during the conditioning phase. These doses were chosen on the basis of previous studies showing that C57BL/6JIco mice display a stronger CPP at a cocaine dose of 20 mg/kg (30,31) and a trend toward aversion in CPA test at a LiCl dose of 3.0 meq/kg (32). For animals in the control group, both chambers were paired with saline.…”

Section: Methodsmentioning

confidence: 99%

Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli

Ventura

Morrone

Puglisi-Allegra

2007

Proc. Natl. Acad. Sci. U.S.A.

169

179

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Recent evidence suggests that rewarding and aversive stimuli affect the same brain areas, including medial prefrontal cortex and nucleus accumbens. Although nucleus accumbens is known to respond to salient stimuli, regardless of their hedonic valence, with selective increased dopamine release, little is known about the role of prefrontal cortex in reward-and aversion-related motivation or about the neurotransmitters involved. Here we find that selective norepinephrine depletion in medial prefrontal cortex of mice abolished the increase in the release of norepinephrine by prefrontal cortex and of dopamine by nucleus accumbens that is induced by food, cocaine, or lithium chloride and impaired the place conditioning induced by both lithium chloride (aversion) and food or cocaine (preference). This is evidence that prefrontal cortical norepinephrine transmission is necessary for motivational salience attribution to both reward-and aversion-related stimuli through modulation of dopamine in nucleus accumbens, a brain area involved in all motivated behaviors. motivation ͉ norepinephrine ͉ prefrontal cortex ͉ dopamine ͉ place conditioning

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Section: Methodsmentioning

confidence: 99%

Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli

Ventura

Morrone

Puglisi-Allegra

2007

Proc. Natl. Acad. Sci. U.S.A.

169

179

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“…Inbred mouse strains do differ in a number of drug related phenotypes [43][44][45][46][47][48]. Many of these phenotypes have now been studied in "quantitative trait locus" paradigms.…”

Section: B Studies Of Murine Strain Differences In Drug Related Phenmentioning

confidence: 99%

“…There is thus some rationale for seeking addiction-associated variants in murine genes that have survived selection pressures on mice as potential models for common addiction-associated human variants that have also survived evolutionary selection pressures on humans. If there are a limited number of genes that can contain variants likely to influence vulnerability to addiction, not provide lethality and not provide strong negative selection, some of these genes from such a group may be more likely than a random group of genes to contain both murine strain differences and common human allelic variants that influence addiction phenotypes.Inbred mouse strains do differ in a number of drug related phenotypes [43][44][45][46][47][48]. Many of these phenotypes have now been studied in "quantitative trait locus" paradigms.…”

mentioning

confidence: 99%

“Higher order” addiction molecular genetics: Convergent data from genome-wide association in humans and mice

Uhl

Drgon

Johnson

et al. 2008

Biochemical Pharmacology

127

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Family, adoption and twin data each support substantial heritability for addictions. Most of this heritable influence is not substance-specific. The overlapping genetic vulnerability for developing dependence on a variety of addictive substances suggests large roles for "higher order" pharamacogenomics in addiction molecular genetics. We and others have now completed genomewide association (GWA) studies of DNAs from individuals with dependence on a variety of addictive substances vs appropriate controls. Recently reported replicated GWA observations identify a number of genes based on comparisons between controls and European-American and African-American polysubstance abusers. Here we review the convergence between these results and data that compares control samples and a) alcohol dependent European Americans, b) methamphetamine dependent Asians and c) nicotine dependent samples from European backgrounds. We also compare these human data to quantitative trait locus (QTL) results from studies of addiction-related phenotypes in mice that focus on alcohol, methamphetamine and barbiturates. These comparisons support a genetic architecture built from largely-polygenic contributions of common allelic variants to dependence on a variety of legal and illegal substances. Many of the gene variants identified in this way are likely to alter specification and maintenance of neuronal connections. KeywordsAssociation genome scanning; substance dependence; microarray; pooled; neuronal connections * To whom correspondence should be addressed at: Molecular Neurobiology, Box 5180, Baltimore, MD 21224 phone: (410) 550-2843 x 146, fax: (410) 550-1535, guhl@intra.nida.nih.gov. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access A. Studies of human addiction vulnerabilitiesVulnerability to addictions is a complex trait with strong genetic influences that are largely shared by abusers of different legal and illegal addictive substances [1][2][3][4]. This conclusion comes from family, adoption and twin studies. Family studies clearly document that first degree relative (eg sibs) of addicts display greater risk for developing substance dependence than more distant relatives [1,5]. Adoption studies consistently find greater similarities between substance abuse phenotypes with biological relatives than with adoptive family members [1]. In twin studies, differences in concordance between genetically identical and fraternal twins also support heritability for vulnerability to addictions [3,[6][7][8][9][10][11][12]. Twin data allows quantitation of the amount, about 50%, of ad...

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“…It is well documented that the D2 inbred strain is resistant to the locomotor stimulant effects of opioid agonists, including morphine (Belknap et al, 1989(Belknap et al, , 1998Orsini et al, 2005;Fadda et al, 2005;Cunningham et al, 1992;Gwynn and Domino, 1984;Hynes and Berkowitz, 1982;Collins and Whitney, 1978;Brase et al, 1977), heroin (Bailey et al, 2010;Castellano et al, 1976), and methadone (Middaugh and Zemp, 1976). We confirmed this lack of sensitivity to fentanyl-induced locomotor activity in D2 mice, and thus only examined fentanyl sensitivity in B6.D2 Csnk1e mice and their B6.B6 Csnk1e wild-type littermates.…”

Section: Fentanyl Sensitivity In B6d2 Csnk1e Micementioning

confidence: 99%

Csnk1e Is a Genetic Regulator of Sensitivity to Psychostimulants and Opioids

Bryant

Parker

Zhou

et al. 2011

Neuropsychopharmacol

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Csnk1e, the gene encoding casein kinase 1-epsilon, has been implicated in sensitivity to amphetamines. Additionally, a polymorphism in CSNK1E was associated with heroin addiction, suggesting that this gene may also affect opioid sensitivity. In this study, we first conducted genome-wide quantitative trait locus (QTL) mapping of methamphetamine (MA)-induced locomotor activity in C57BL/6J (B6) Â DBA/ 2J (D2)-F 2 mice and a more highly recombinant F 8 advanced intercross line. We identified a QTL on chromosome 15 that contained Csnk1e (63-86 Mb; Csnk1e ¼ 79.25 Mb). We replicated this result and further narrowed the locus using B6.D2 Csnk1e and D2.B6 Csnk1e reciprocal congenic lines (78-86.8 and 78.7-81.6 Mb, respectively). This locus also affected sensitivity to the m-opioid receptor agonist fentanyl. Next, we directly tested the hypothesis that Csnk1e is a genetic regulator of sensitivity to psychostimulants and opioids. Mice harboring a null allele of Csnk1e showed an increase in locomotor activity following MA administration. Consistent with this result, coadministration of a selective pharmacological inhibitor of Csnk1e (PF-4800567) increased the locomotor stimulant response to both MA and fentanyl. These results show that a narrow genetic locus that contains Csnk1e is associated with differences in sensitivity to MA and fentanyl. Furthermore, gene knockout and selective pharmacological inhibition of Csnk1e define its role as a negative regulator of sensitivity to psychostimulants and opioids.

show abstract

Susceptibility to conditioned place preference induced by addictive drugs in mice of the C57BL/6 and DBA/2 inbred strains

Abstract: The results demonstrate that C57 and DBA mice differ in their sensitivity to cocaine- and morphine-induced CPP and suggest that the two strains differ in sensitivity to the positive incentive properties of drugs of abuse.

Cited by 102 publications

References 34 publications

Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli

Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli

“Higher order” addiction molecular genetics: Convergent data from genome-wide association in humans and mice

Csnk1e Is a Genetic Regulator of Sensitivity to Psychostimulants and Opioids

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