Possible role of norepinephrine in cocaine-induced conditioned taste aversions

Serafine, Katherine M.; Riley, Anthony L.

doi:10.1016/j.pbb.2008.10.019

Cited by 19 publications

(30 citation statements)

References 46 publications

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“…Although the mechanism underlying the US preexposure effect (either with the same or different drugs) is not fully characterized, for some drugs, e.g., alcohol, nicotine and morphine, it is thought that changes to the drug during preexposure impact the effects of that (or a different drug) at conditioning, weakening its ability to induce aversions (Barker and Johns, 1978, Berman and Cannon, 1974, Hunt et al , 1985, Iwamoto and Williamson, 1984, Simpson and Riley, 2005). The impact of preexposure in the cross-drug design is generally thought to be the result of the development of tolerance to common aversive effects shared by the drugs, presumably due to some common mechanism of action (Riley and Simpson, 2001: Serafine and Riley 2009: Serafine and Riley 2010). It is interesting to note that the cross-drug preexposure effect has been previously reported with nicotine and alcohol (Kunin et al , 1999).…”

Section: Discussionmentioning

confidence: 99%

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Rinker

Hutchison

Chen

et al. 2011

Pharmacology Biochemistry and Behavior

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The majority of smokers begin their habit during adolescence, which often precedes experimentation with alcohol. Interestingly, very little preclinical work has been done examining how exposure to nicotine during periadolescence impacts the affective properties of alcohol in adulthood. Understanding how periadolescent nicotine exposure influences the aversive effects of alcohol might help to explain why it becomes more acceptable to this preexposed population. Thus, Experiment 1 exposed male Sprague Dawley rats to either saline or nicotine (0.4 mg/kg, IP) from postnatal day 34 to 43 (periadolescence) and then examined changes in the aversive effects of alcohol (0, 0.56, 1.0 and 1.8 g/kg, IP) in adulthood using the conditioned taste aversion (CTA) design. Changes in blood alcohol concentration (BAC) as well as alcohol-induced hypothermia and locomotor suppression were also assessed. To determine if changes seen were specific to nicotine exposure during periadolescence, the procedures were replicated in adults (Experiment 2). Preexposure to nicotine during periadolescence attenuated the acquisition of the alcohol-induced CTAs (at 1.0 g/kg) and the hypothermic effects of alcohol (1.0 g/kg). Adult nicotine preexposure produced similar attenuation in alcohol's aversive (at 1.8 g/kg) and hypothermic (1.8 g/kg) effects. Neither adolescent nor adult nicotine preexposure altered BACs or alcohol-induced locomotor suppression. These results suggest that nicotine can alter the aversive and physiological effects of alcohol, regardless of the age at which exposure occurs, possibly increasing its overall reinforcing value and making it more likely to be consumed.

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Section: Discussionmentioning

confidence: 99%

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Rinker

Hutchison

Chen

et al. 2011

Pharmacology Biochemistry and Behavior

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“…Cortical dopamine fiber densities were examined in 50-μm coronal vibratome sections cut through six levels of frontal cortices (bregma +1.38 to +0.68 mm) of and two-bottle testing, as described (23). After acclimation, handling and 20 min/d access to water, mice were given four series of 20-min conditioning sessions during which they were provided access to 1 g/L saccharin solution, then injected within 20 min with 0, 5, 10 or 20 mg/kg cocaine i.p., then 2 d of water recovery.…”

Section: Methodsmentioning

confidence: 99%

Cadherin 13: Human cis-Regulation and Selectively Altered Addiction Phenotypes and Cerebral Cortical Dopamine in Knockout Mice

Drgonová

Walther

Hartstein

et al. 2016

Mol Med

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The cadherin 13 (CDH13) gene encodes a cell adhesion molecule likely to influence development and connections of brain circuits that modulate addiction, locomotion and cognition, including those that involve midbrain dopamine neurons. Human CDH13 mRNA expression differs by more than 80% in postmortem cerebral cortical samples from individuals with different CDH13 genotypes, supporting examination of mice with altered CDH13 expression as models for common human variation at this locus. Constitutive CDH13 knockout mice display evidence for changed cocaine reward: shifted dose response relationship in tests of cocaine-conditioned place preference using doses that do not alter cocaine-conditioned taste aversion. Reduced adult CDH13 expression in conditional knockouts also alters cocaine reward in ways that correlate with individual differences in cortical CDH13 mRNA levels. In control and comparison behavioral assessments, knockout mice display modestly quicker acquisition of rotarod and water maze tasks, with a trend toward faster acquisition of 5-choice serial reaction time tasks that otherwise displayed no genotype-related differences. They display significant differences in locomotion in some settings, with larger effects in males. In assessments of brain changes that might contribute to these behavioral differences, there are selective alterations of dopamine levels, dopamine/metabolite ratios, dopaminergic fiber densities and mRNA encoding the activity dependent transcription factor npas4 in cerebral cortex of knockout mice. These novel data and previously reported human associations of CDH13 variants with addiction, individual differences in responses to stimulant administration and attention deficit hyperactivity disorder (ADHD) phenotypes suggest that levels of CDH13 expression, through mechanisms likely to include effects on mesocortical dopamine, influence stimulant reward and may contribute modestly to cognitive and locomotor phenotypes relevant to ADHD.

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“…In other work assessing the effects of cross-drug preexposure on aversion learning, both attenuating and potentiating effects have been reported. That is, preexposure to Compound A can weaken or strengthen the aversion induced by Compound B (De Beun et al, 1996; Gommans et al, 1998; Serafine and Riley, 2009; see also Riley and Simpson, 2001). Since preexposure can result in either effect, it is necessary to use doses during conditioning that induce intermediate aversions (to detect potentiation or attenuation).…”

Section: Methodsmentioning

confidence: 99%

“…This prediction is based on work utilizing the cross-drug preexposure preparation (De Beun et al, 1996; Gommans et al, 1998; Serafine and Riley, 2009) in which exposure to one compound is given prior to aversion conditioning with another. Under such conditions, aversions to the second compound are often weakened, an effect commonly interpreted as being due to cross tolerance (or adaptation) to the shared aversion-inducing effects of the two drugs (Berman and Cannon, 1974; Jones et al, 2009; LeBlanc and Cappell, 1974; Simpson and Riley, 2005; Serafine and Riley, 2009; 2010; for reviews and alternative interpretations, see Cappell and LeBlanc, 1977; Randich and LoLordo, 1979; Riley and Simpson, 2001). In one of the first demonstrations of the use of this procedure for investigations of common stimulus properties, De Beun and colleagues (1993) reported that CTAs induced by the selective serotonin (5-HT) agonist 8-OHDPAT were blocked by preexposure to compounds that also had 5-HT agonist activity (for the same receptor subtype, e.g., 5-HT 1A ; see De Beun et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

“…Given that these compounds (ipsapirone, buspirone, RU-24969, sertraline, d-amphetamine, LSD, metergoline and idazoxane) were effective in blocking 8-OHDPAT-induced CTAs, De Beun and colleagues concluded that cross-drug preexposure could be used to assess the commonalities in aversion-inducing mechanism between different compounds (De Beun et al, 1993). Since this demonstration, several other investigations have also utilized this procedure to examine common mechanisms in the aversive effects of various compounds (see De Beun et al, 1996; Gommans et al, 1998; Jones et al, 2009; Kayir et al, 2008; Olivier et al, 1999; Van Hest et al, 1992; Serafine and Riley, 2009; 2010). …”

Section: Introductionmentioning

confidence: 99%

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Dopamine mediates cocaine-induced conditioned taste aversions as demonstrated with cross-drug preexposure to GBR 12909

Serafine

Briscione

Rice

et al. 2012

Pharmacology Biochemistry and Behavior

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Although cocaine readily induces taste aversions, little is known about the mechanisms underlying this effect. It has been suggested that its inhibitory effects at one of the monoamine transporters may be mediating this suppression. Using the cross-drug preexposure preparation, the present series of studies examined a possible role of dopamine (DA) in this effect. Male Sprague-Dawley rats were exposed to cocaine (18 mg/kg; Experiment 1) or the selective DA transporter (DAT) inhibitor GBR 12909 (50 mg/kg; Experiment 2) prior to the pairing of a novel saccharin solution with injections of GBR 12909 (32 mg/kg), cocaine (18 mg/kg) or vehicle in a conditioned taste aversion (CTA) procedure. Preexposure to cocaine attenuated aversions induced by itself but not aversions induced by GBR 12909 (Experiment 1). Conversely, preexposure to GBR 12909 attenuated aversions induced by itself and cocaine (Experiment 2). This asymmetry suggests that cocaine and GBR 12909 induce CTAs via similar, but non-identical, mechanisms. These data are discussed in the context of previous work demonstrating roles for dopamine, norepinephrine and serotonin in cocaine-induced CTAs.

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Possible role of norepinephrine in cocaine-induced conditioned taste aversions

Cited by 19 publications

References 46 publications

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Cadherin 13: Human cis-Regulation and Selectively Altered Addiction Phenotypes and Cerebral Cortical Dopamine in Knockout Mice

Dopamine mediates cocaine-induced conditioned taste aversions as demonstrated with cross-drug preexposure to GBR 12909

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