Morphine-induced suppression of saccharin intake is correlated with elevated corticosterone levels

Gomez, Felipe; Leo, Nicole A; Grigson, Patricia S.

doi:10.1016/s0006-8993(00)02093-x

Cited by 34 publications

(49 citation statements)

References 38 publications

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“…While negative contrast (reward devaluation) may contribute to this finding with dopamine [70], this blunting also could be explained by the onset of cue-induced craving and/ or withdrawal because accumbens dopamine levels also are blunted following the onset of naltrexone-induced withdrawal [71]. Second, using experimenter-delivered drug, we have found large individual differences whereby some rats are more likely to avoid intake of the drug-associated taste cue than are others and greater avoidance of the taste cue is associated with greater cue-induced elevation of circulating corticosterone [72]. As with the dopamine data, the conditioned elevation in circulating corticosterone also could be interpreted as evidence of cue-induced craving and/or withdrawal because circulating corticosterone levels are known to be elevated during naloxone-precipitated withdrawal [73].…”

Section: The Model: Experimenter Delivered Drugmentioning

confidence: 81%

“…As shown previously with slightly different procedures [24], rats suppressed intake of the saccharin CS following repeated daily pairings with self-administered cocaine. Moreover, as with the passive administration of drug [72], individual differences were evident whereby some rats (referred to as large suppressers) were more likely than others (referred to as the small suppressers) to avoid intake of the saccharin cue following daily saccharin-cocaine pairings. These individual differences in intake of the CS also were accompanied by individual differences in 'intake' of the drug.…”

Section: The Model: Drug Self-administrationmentioning

confidence: 99%

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Reward comparison: the Achilles’ heel and hope for addiction

Grigson

2008

Drug Discovery Today: Disease Models

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In the words of the late Charles Flaherty, reward comparison is commonplace. Rats and man, it appears, compare all rewards and this capacity likely contributes to our ability to select the most appropriate reward/behavior (food, water, salt, sex), at the most ideal level (e.g., a certain sweetness), at any given time. A second advantage of our predisposition for reward comparison is that the availability of rich alternative rewards can protect against our becoming addicted to any single reward/behavior. Thus, the potential protective effects of natural rewards/enrichment are addressed. Despite this, behavior can become inflexible when, through the development of addiction, stress, drug, or cues elicit craving, withdrawal, and ultimately, drug-seeking. Drug-seeking corresponds with a 'window of inopportunity', when even potent natural rewards have little or no impact on behavior. During this time, there is a unitary solution to the need state, and that solution is drug. The present animal model explores this 'window of inopportunity' when natural rewards are devalued and drug-seeking is engaged and considers a mode of possible intervention.

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Section: The Model: Experimenter Delivered Drugmentioning

confidence: 81%

Section: The Model: Drug Self-administrationmentioning

confidence: 99%

Reward comparison: the Achilles’ heel and hope for addiction

Grigson

2008

Drug Discovery Today: Disease Models

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“…Mice and rats avoid intake of a palatable natural reward (such as saccharin) when paired with a drug of abuse such as cocaine (Cappell et al , 1973, Carey and Goodall, 1974, Goudie et al , 1978). Data demonstrate greater drug-induced suppression of saccharin intake is correlated with greater cocaine self-administration (Grigson and Twining, 2002) and elevated corticosterone levels (Gomez et al , 2000) and a single saccharin-morphine pairing blunts accumbens dopamine release in response to saccharin (Grigson and Hajnal, 2007). While dopamine and drug-induced suppression has received a fair amount of attention, the present study represents an initial examination into the relatively unexplored role of glutamate signaling and homeostasis in this model.…”

Section: Introductionmentioning

confidence: 99%

Ceftriaxone attenuates acquisition and facilitates extinction of cocaine-induced suppression of saccharin intake in C57BL/6J mice

Freet

Lawrence

2015

Physiology & Behavior

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Growing evidence implicates glutamate homeostasis in a number of behaviors observed in addiction such as acquisition of drug taking, motivation, and reinstatement. To date, however, the role of glutamate homeostasis in the avoidance of natural rewards due to exposure to drugs of abuse has received little attention. The aim of the current study was to evaluate the beta-lactam antibiotic, ceftriaxone, which has been shown to normalize disrupted glutamate homeostasis associated with exposure to drugs of abuse, in cocaine-induced suppression of saccharin intake in C57BL/6J mice. Briefly, C57BL/6J mice received daily injections of either 200 mg/kg ceftriaxone or saline. Mice were then given access to 0.15% saccharin for 1 hour and immediately injected intraperitoneally with either saline or 30 mg/kg cocaine; taste-drug pairings occurred every 24 hours for 5 trials followed by a final CS only trial. One week following taste-drug pairings, extinction was evaluated in a series of one- and two-bottle saccharin intake tests. Individual differences in cocaine-induced suppression were observed (i.e., low and high suppressors) with differential effects of ceftriaxone. Ceftriaxone delayed suppression of saccharin intake in high suppressors but prevented suppression in low suppressors. In addition, ceftriaxone history facilitated extinction in the high suppressors. These data suggest that changes in glutamate homeostasis may be involved in the formation and expression of cocaine-induced suppression of saccharin intake in mice.

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“…Thus, like conditioned withdrawal (Coffey et al, 2013; Hotsenpiller, Giorgetti, & Wolf, 2001; McDonald, Parker, & Siegel, 1997), avoidance of the taste cue also is accompanied by elevated levels of circulating corticosterone (Gomez, Leo, & Grigson, 2000), blunted (Grigson & Hajnal, 2007) or even reversed (i.e., reduced below baseline) (Wheeler et al, 2011) levels of accumbens dopamine, and the onset of aversive taste reactivity (TR) behavior (e.g., gapes) following the intraoral delivery of the drug-paired taste cue (Wheeler et al, 2008). Importantly, greater avoidance of the taste cue (Grigson & Twining, 2002; Twining, Bolan, & Grigson, 2009), and a greater reduction in accumbens dopamine (Wheeler et al, 2011), reliably predict greater drug taking in rats.…”

mentioning

confidence: 99%

Once is too much: Conditioned aversion develops immediately and predicts future cocaine self-administration behavior in rats.

Colechio

Imperio

Grigson

2014

Behavioral Neuroscience

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Rats emit aversive taste reactivity (TR) behavior (i.e., gapes) following intraoral delivery of a cocaine-paired taste cue and greater conditioned aversive TR at the end of training predicts greater drug-seeking and taking. Here, we examined the development of this conditioned aversive TR behavior on a trial by trial basis in an effort to determine when the change in behavior occurs and whether early changes in this behavior can be used to predict later drug-taking. The results show that conditioned aversive TR to a cocaine-paired cue occurs very early in training (i.e., following as few as 1 – 2 taste-drug pairings) and, importantly, that it can be used to predict later drug-seeking and drug-taking in rats.

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Morphine-induced suppression of saccharin intake is correlated with elevated corticosterone levels

Cited by 34 publications

References 38 publications

Reward comparison: the Achilles’ heel and hope for addiction

Reward comparison: the Achilles’ heel and hope for addiction

Ceftriaxone attenuates acquisition and facilitates extinction of cocaine-induced suppression of saccharin intake in C57BL/6J mice

Once is too much: Conditioned aversion develops immediately and predicts future cocaine self-administration behavior in rats.

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