Saccharin's rewarding, conditioned reinforcing, and memory-improving properties: Mediation by isomorphic or independent processes?

Stefurak, Taresa L.; Kooy, Derek van der

doi:10.1037/0735-7044.106.1.125

Cited by 26 publications

(22 citation statements)

References 74 publications

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“…The most striking difference between gp120‐tg and non‐tg mice was in their preference for the highly palatable reinforcer saccharin, with gp120‐tg mice showing greater saccharin preference and consumption compared with non‐tg mice. Saccharin is naturally rewarding to rodents due almost exclusively to its sweet taste (Stefurak & van der Kooy ). Interestingly, saccharin consumption has been shown to be a predictor of the development of drug and alcohol dependence in rats (Gosnell et al .…”

Section: Discussionmentioning

confidence: 99%

Expression of HIV gp120 protein increases sensitivity to the rewarding properties of methamphetamine in mice

et al. 2012

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Methamphetamine abuse and human immunodeficiency virus (HIV) infection induce neuropathological changes in corticolimbic brain areas involved in reward and cognitive function. Little is known about the combined effects of methamphetamine and HIV infection on cognitive and reward processes. The HIV/gp120 protein induces neurodegeneration in mice, similar to HIV-induced pathology in humans. We investigated the effects of gp120 expression on associative learning, preference for methamphetamine and non-drug reinforcers, and sensitivity to the conditioned rewarding properties of methamphetamine in transgenic (tg) mice expressing HIV/gp120 protein (gp120-tg). gp120-tg mice learned the operant response for food at the same rate as non-tg mice. In the two-bottle choice procedure with restricted access to drugs, gp120-tg mice exhibited greater preference for methamphetamine and saccharin than non-tg mice, whereas preference for quinine was similar between genotypes. Under conditions of unrestricted access to methamphetamine, the mice exhibited a decreased preference for increasing methamphetamine concentrations. However, male gp120-tg mice showed a decreased preference for methamphetamine at lower concentrations than non-tg male mice. gp120-tg mice developed methamphetamine-induced conditioned place preference at lower methamphetamine doses compared with non-tg mice. No differences in methamphetamine pharmacokinetics were found between genotypes. These results indicate that gp120-tg mice exhibit no deficits in associative learning or reward/motivational function for a natural reinforcer. Interestingly, gp120 expression resulted in increased preference for methamphetamine and a highly palatable non-drug reinforcer (saccharin) and increased sensitivity to methamphetamine-induced conditioned reward. These data suggest that HIV-positive individuals may have increased sensitivity to methamphetamine, leading to high methamphetamine abuse potential in this population.

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Section: Discussionmentioning

confidence: 99%

Expression of HIV gp120 protein increases sensitivity to the rewarding properties of methamphetamine in mice

et al. 2012

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“…Numerous studies have shown that previous exposure to natural reward or addictive drugs can cross-sensitize animals to other addictive substances through the common reward circuits (Itzhak and Martin, 1999; Biala and Weglinska, 2004; Clark and Bernstein, 2006; Avena et al, 2008). High concentrations of saccharin, despite the aversive taste, have strong rewarding, conditioned reinforcing, and memory-improving properties (Stefurak and van der Kooy, 1992). Therefore, it is likely that a high concentration of saccharin functions as an addictive substance, sensitizing the rewarding neuronal circuits.…”

Section: Discussionmentioning

confidence: 99%

CD-1 mice show individual differences in nicotine preference in a modified two-bottle oral self-administration model

Cao

Gautier

2012

Front. Mol. Neurosci.

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Although both animal and human studies reveal significant contributions of genetics to smoking addiction, many human studies were underpowered or biased by potential confounding variables, and animal genetic studies are challenged by limited genetic variations and lack of convincing phenotypes. To address these concerns, we used non-sibling outbred CD-1 mice to evaluate individual differences in nicotine preference with a modified two-bottle oral self-administration model. Animals were first given free access to two bottles, one filled with nicotine dissolved in 2% saccharin and the other with saccharin only. Under this regular two-bottle choice condition, the majority of animals avoided the nicotine solution with limited individual differences. However, when we modified the model by introducing 4 days of exposure to 5% saccharin in the drinking water, the animals significantly increased nicotine consumption in the two-bottle choice test, with about 30% animals showing a nicotine preference. Nicotine preference after 5% saccharin treatment remained elevated throughout the 28 days of the experiment. Further, we found there existed striking individual differences in nicotine consumption after exposure to 5% saccharin, with a range of 0–100% of total liquid consumption. The enhanced individual differences and the ratio of nicotine consumption were observed at different concentrations of nicotine (10–80 μg/ml) and in both adolescents and adults. Further examination on the induction mechanism showed that the long-lasting nicotine preference was not correlated with nicotine consumption before the induction, 5% saccharin consumption, or weight gain during the induction. Although liquid consumption during the 4 days of 5% saccharin exposure was decreased by about 30%, comparable liquid restriction alone for 4 days did not induce nicotine preference. Together, this study showed a strong and stable nicotine preference in CD-1 mice, which was induced by a short-term high concentration of saccharin in the drinking water. Considering the nature and heterogeneity of CD-1 mice, the striking individual differences imply that genetics plays an important role in nicotine preference observed in these animals.

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“…The solutions tested in the two-bottle consumption studies were 5% sucrose, which is palatable and nutritive, as well as 0.1% saccharin and 0.6% saline, which are also tasteful for rats but are not nutritive (Fregly and Rowland 1992; Hausmann 1933; McHugh 1979; Stefurak and van der 1992; Warwick and Weingarten 1996). Consistent with previous reports (Fregly and Rowland 1992; Hausmann 1933; Hayward et al 2006; Stewart et al 1994), under basal conditions, all three palatable fluids were preferred to water; however, sucrose, at the concentrations used, was consumed more avidly than the two other solutions.…”

Section: Discussionmentioning

confidence: 99%

18-Methoxycoronaridine: a potential new treatment for obesity in rats?

et al. 2008

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Rationale Excessive eating often leads to obesity. Although a variety of neurotransmitters and brain regions are involved in modulating food intake, a role of accumbal dopamine is thought to be critical for several aspects of this behavior. Since 18-methoxycoronaridine (18-MC), a selective antagonist of α3β4 nicotinic receptors, was previously shown to alter dopamine release in the nucleus accumbens in response to chronic injections of cocaine and morphine, this drug could be a promising therapy for abnormal eating behavior. Objectives Assess the effect of 18-MC on the consumption of sucrose (15%) vs. water in a self-administration paradigm and on the intake of freely available palatable fluids (i.e., 5% sucrose, 0.1% saccharin, and 0.6% saline solutions) as well as on water intake. Determine whether repeated administration of 18-MC (20 mg/kg i.p.) affects weight gain, food intake, and fat deposition in rats drinking 30% sucrose solution. Results Acute administration of 18-MC (10–40 mg/kg i.p.) reduced operant responding for sucrose and decreased ad libitum ingestion of sucrose, saccharin, and saline. The highest dose of 18-MC also reduced consumption of water when palatable fluids were not available. In rats having unlimited access to sucrose (30%), chronic treatment with 18-MC (20 mg/kg i.p.) prevented sucrose-induced increases in body weight, decreased fat deposition, and reduced consumption of sucrose while not altering food intake. Conclusions These data suggest that antagonism of α3β4 nicotinic receptors may be involved in the regulation of intake of palatable substances regardless of its caloric value and may participate in maintaining obesity.

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Saccharin's rewarding, conditioned reinforcing, and memory-improving properties: Mediation by isomorphic or independent processes?

Cited by 26 publications

References 74 publications

Expression of HIV gp120 protein increases sensitivity to the rewarding properties of methamphetamine in mice

Expression of HIV gp120 protein increases sensitivity to the rewarding properties of methamphetamine in mice

CD-1 mice show individual differences in nicotine preference in a modified two-bottle oral self-administration model

18-Methoxycoronaridine: a potential new treatment for obesity in rats?

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