Conditioned taste aversion in rats for a threonine-deficient diet

Feurté, Sébastien; Nicolaı̈dis, Stylianos; Berridge, Kent

doi:10.1016/s0031-9384(99)00202-4

Cited by 30 publications

(13 citation statements)

References 47 publications

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“…positive tongue protrusion and lip licking to sweetness versus aversive gapes to bitterness) that are homologous to human infant affective facial expressions elicited by tastes [2, 4, 28]. [22] We tested for hedonic enhancement in a standard taste reactivity test using a sucrose solution infused directly in the mouth to control stimulus quality and duration, and separately for the taste of sweet/fatty chocolate as rats voluntarily ate 0.2 g fragments of M&Ms™, replicating the chocolate stimulus and conditions of eating enhancement [29]. Taste reactivity results of both tests showed that DAMGO microinjections in anterior dorsomedial neostriatum failed to enhance positive hedonic taste reactions at all, either to oral infusions of 1% sucrose solution (F (3,9) =1.875, p=.204; Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Orofacial reactions elicited by sucrose taste (1% sucrose solution) were video recorded in a standard taste reactivity test [2, 4]. Orofacial reactions elicited by the combined sweet/fatty sensations of milk chocolate were video recorded in a voluntary ingestion modification of the taste reactivity paradigm, in which the rat was given fragments of chocolate M&Ms™ (0.2 g each) and allowed to eat voluntarily and emit postprandial hedonic reactions for 6s after each fragment (scoring was controlled for facial visibility)[29]. All behaviors were scored off line in slow motion by an observer blind to DAMGO/vehicle condition (frame-by-frame to 1/10 th speed).…”

Section: Methodsmentioning

confidence: 99%

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Enkephalin Surges in Dorsal Neostriatum as a Signal to Eat

et al. 2012

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Summary Compulsive over-consumption of rewards characterizes disorders ranging from binge eating to drug addiction. Here, we provide evidence that enkephalin surges in an anteromedial quadrant of dorsal neostriatum contribute to generating intense consumption of palatable food. In ventral striatum, mu opioid circuitry contributes an important component of motivation to consume rewards [1–4]. In dorsal neostriatum, mu opioid receptors are concentrated within striosomes that receive inputs from limbic regions of prefrontal cortex [5–13]. We employed advanced opioid microdialysis techniques that allow detection of extracellular enkephalin levels. Endogenous >150% enkephalin surges in anterior dorsomedial neostriatum were triggered as rats began to consume palatable chocolates. By contrast, dynorphin levels remained unchanged. Further, a causal role for mu opioid stimulation in over-consumption was demonstrated by observations that microinjection in the same anterior dorsomedial quadrant of a mu receptor agonist (DAMGO) generated intense >250% increases in intake of palatable sweet food (without altering hedonic impact of sweet tastes). Mapping by “Fos plume” methods confirmed the hyperphagic effect to be anatomically localized to the anterior medial quadrant of the dorsal neostriatum, whereas other quadrants were relatively ineffective. These findings reveal that opioid signals in anteromedial dorsal neostriatum are able to code and cause motivation to consume sensory rewards.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Enkephalin Surges in Dorsal Neostriatum as a Signal to Eat

et al. 2012

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“…Instead of delivering the tastants through intraoral cannulas, a 200-l volume of sucrose solution was placed on the transparent floor of a cylindrical test cage, and the rat's orofacial expressions were videotaped from below after bouts of voluntary intake. Voluntary intake has been applied previously to the taste reactivity test to measure "liking" in rats and mice (27,51,52). We initially used intraoral fistulas for the delivery of tastants, but we switched to voluntary intake because of problems with patency and because we did not find significant differences in the monotonic increase of positive hedonic reactions in a subset of lean rats.…”

Section: Methodsmentioning

confidence: 99%

“Liking” and “wanting” of sweet and oily food stimuli as affected by high-fat diet-induced obesity, weight loss, leptin, and genetic predisposition

Shin

Townsend

Patterson

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Cross-sectional studies in both humans and animals have demonstrated associations between obesity and altered reward functions at the behavioral and neural level, but it is unclear whether these alterations are cause or consequence of the obese state. Reward behaviors were quantified in male, outbred Sprague-Dawley (SD) and selected line obesity-prone (OP) and obesity-resistant (OR) rats after induction of obesity by high-fat diet feeding and after subsequent loss of excess body weight by chronic calorie restriction. As measured by the brief access lick and taste-reactivity paradigms, both obese SD and OP rats "liked" low concentrations of sucrose and corn oil less, but "liked" the highest concentrations more, compared with lean rats, and this effect was fully reversed by weight loss in SD rats. Acute food deprivation was unable to change decreased responsiveness to low concentrations but eliminated increased responsiveness to high concentrations in obese SD rats, and leptin administration in weight-reduced SD rats shifted concentration-response curves toward that seen in the obese state in the brief access lick test. "Wanting" and reinforcement learning as assessed in the incentive runway and progressive ratio lever-pressing paradigms was paradoxically decreased in both obese (compared with lean SD rats) and OP (compared with OR rats). Thus, reversible, obesity-associated, reduced "liking" and "wanting" of low-calorie foods in SD rats suggest a role for secondary effects of the obese state on reward functions, while similar differences between select lines of OP and OR rats before induction of obesity indicate a genetic component.

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“…Like other researchers (e.g., Feurte, Nicolaidis, & Berridge, 2000; Garcia et al, 1970; Pelchat & Rozin, 1982), we view CTA as a palatability downshift mechanism and consider the traditional index of CTA, reduced intake, to be a consequence of the conditioned palatability downshift. Thus, in the context of CTA acquisition, reductions of intake can be viewed as a good proxy for the conditioned reduction in taste palatability.…”

Section: Characteristics Of Conditioned Taste Aversionmentioning

confidence: 99%

Conditioned taste aversions: From poisons to pain to drugs of abuse

2016

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Learning what to eat and what not to eat is fundamental to our well-being, quality of life and survival. In particular, the acquisition of conditioned taste aversions (CTAs) protects all animals (including humans) against ingesting foods that contain poisons or toxins. Counterintuitively, CTAs can also develop in situations where we know with absolute certainty that the food did not cause the subsequent aversive systemic effect. Recent non-human animal research, analyzing palatability shifts, indicates that a wider range of stimuli than traditionally acknowledged can induce CTAs. This article integrates these new findings with a reappraisal of some known characteristics of CTA, and presents a novel conceptual analysis that is broader and more comprehensive than other accounts of CTA learning.

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Conditioned taste aversion in rats for a threonine-deficient diet

Cited by 30 publications

References 47 publications

Enkephalin Surges in Dorsal Neostriatum as a Signal to Eat

Enkephalin Surges in Dorsal Neostriatum as a Signal to Eat

“Liking” and “wanting” of sweet and oily food stimuli as affected by high-fat diet-induced obesity, weight loss, leptin, and genetic predisposition

Conditioned taste aversions: From poisons to pain to drugs of abuse

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