The taste reactivity test. I. Mimetic responses to gustatory stimuli in neurologically normal rats

Grill, Harvey J.; Norgren, Ralph

doi:10.1016/0006-8993(78)90568-1

Cited by 1,104 publications

(782 citation statements)

References 16 publications

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“…Experiment 4 studied the effects of AM4113 on the consumption of diets with different macronutrient compositions (eg high fat, high carbohydrate, and lab chow; McLaughlin et al, 2003McLaughlin et al, , 2005bMcLaughlin et al, , 2006. Finally, experiment 5 employed the taste reactivity test developed by Grill and Norgren (1978) to determine if AM4113 can produce conditioned gaping in a manner similar to that previously shown to occur after administration of AM251 (McLaughlin et al, 2005b). It was hypothesized that AM4113 would display neurochemical characteristics of a CB1 neutral antagonist without inverse agonist properties, would be able to block behavioral effects of a CB1 agonist, and would attenuate appetite and foodreinforced behaviors without inducing behaviors associated with nausea and malaise.…”

Section: Introductionmentioning

confidence: 99%

The Novel Cannabinoid CB1 Receptor Neutral Antagonist AM4113 Suppresses Food Intake and Food-Reinforced Behavior but Does not Induce Signs of Nausea in Rats

Sink

McLaughlin

Wood

et al. 2007

Neuropsychopharmacol

139

189

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Drugs that interfere with cannabinoid CB1 transmission suppress various food-motivated behaviors, and it has been suggested that such drugs could be useful as appetite suppressants. Biochemical studies indicate that most of these drugs assessed thus far have been CB1 inverse agonists, and although they have been shown to suppress food intake, they also appear to induce nausea and malaise. The present studies were undertaken to characterize the behavioral effects of AM4113, which is a CB1 neutral antagonist, and to examine whether this drug can reduce food-reinforced behaviors and feeding on diets with varying macronutrient compositions. Biochemical data demonstrated that AM4113 binds to CB1 receptors, but does not show inverse agonist properties (ie no effects on cyclic-AMP production). In tests of spontaneous locomotion and analgesia, AM4113 reversed the effects of the CB1 agonist AM411. AM4113 suppressed food-reinforced operant responding with rats responding on fixed ratio (FR) 1 and 5 schedules of reinforcement in a dosedependent manner, and also suppressed feeding on high-fat, high-carbohydrate, and lab chow diets. However, in the same dose range that suppressed feeding, AM4113 did not induce conditioned gaping, which is a sign of nausea and food-related malaise in rats. These results suggest that AM4113 may decrease appetite by blocking endogenous cannabinoid tone, and that this drug may be less associated with nausea than CB1 inverse agonists. Neuropsychopharmacology (2008) 33, 946-955;

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Section: Introductionmentioning

confidence: 99%

The Novel Cannabinoid CB1 Receptor Neutral Antagonist AM4113 Suppresses Food Intake and Food-Reinforced Behavior but Does not Induce Signs of Nausea in Rats

Sink

McLaughlin

Wood

et al. 2007

Neuropsychopharmacol

139

189

View full text Add to dashboard Cite

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“…), whereas bitter tastes instead elicit facial 'disliking' expressions (gapes, etc.). These homologousaffective expressions (sharing features such as identical allometric timing laws) seem to have developed from the same evolutionary source in humans, orangutans, chimpanzees, monkeys, and even rats and mice (Grill and Norgren 1978a;Steiner 1973;Steiner et al 2001). Homology in origin of 'liking' reactions implies that the underlying hedonic brain mechanisms are similar in humans and other animals, opening the way for an affective neuroscience of pleasure that bridges both.…”

Section: Pleasure Coding Versus Causalitymentioning

confidence: 99%

Affective neuroscience of pleasure: reward in humans and animals

2008

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Introduction Pleasure and reward are generated by brain circuits that are largely shared between humans and other animals. Discussion Here, we survey some fundamental topics regarding pleasure mechanisms and explicitly compare humans and animals. Conclusion Topics surveyed include liking, wanting, and learning components of reward; brain coding versus brain causing of reward; subjective pleasure versus objective hedonic reactions; roles of orbitofrontal cortex and related cortex regions; subcortical hedonic hotspots for pleasure generation; reappraisals of dopamine and pleasure-electrode controversies; and the relation of pleasure to happiness.

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“…Oral cannulae were inserted lateral to the first maxillary molar, threaded behind the zygomatic arch, and exited through the dorsal head where they were cemented to skull screws (Grill and Norgren, 1978;Berridge et al, 1984). All rats were allowed to recover before testing for at least 7 days after surgery, and were habituated to their taste reactivity or food intake test chambers for 30 min on 4 consecutive days prior to the first test.…”

Section: Surgerymentioning

confidence: 99%

Endocannabinoid Hedonic Hotspot for Sensory Pleasure: Anandamide in Nucleus Accumbens Shell Enhances ‘Liking’ of a Sweet Reward

Mahler

Smith

Berridge

2007

Neuropsychopharmacol

303

258

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Cannabinoid drugs such as D 9 -THC are euphoric and rewarding, and also stimulate food intake in humans and animals. Little is known about how naturally occurring endogenous brain cannabinoids mediate pleasure from food or other natural sensory rewards. The taste reactivity paradigm measures effects of brain manipulations on affective orofacial reactions to intraorally administered pleasant and unpleasant tastes. Here we tested if anandamide microinjection into medial nucleus accumbens shell enhances these affective reactions to sweet and bitter tastes in rats. Anandamide doubled the number of positive 'liking' reactions elicited by intraoral sucrose, without altering negative 'disliking' reactions to bitter quinine. Anandamide microinjections produced Fos plumes of approximately 0.02-1 mm 3 volume. Plume-based maps, integrated with behavioral data, identified the medial shell of accumbens as the anatomical hotspot responsible for hedonic amplification. Anandamide produced especially intense hedonic enhancement in a roughly 1.6 mm 3 'hedonic hotspot' in dorsal medial shell, where anandamide also stimulated eating behavior. These results demonstrate that endocannabinoid signals within medial accumbens shell specifically amplify the positive hedonic impact of a natural reward (though identification of the receptor specificity of this effect will require future studies). Identification of an endocannabinoid hotspot for sensory pleasure gives insight into brain mechanisms of natural reward, and may be relevant to understanding the neural effects of cannabinoid drugs of abuse and therapeutic agents.

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The taste reactivity test. I. Mimetic responses to gustatory stimuli in neurologically normal rats

Cited by 1,104 publications

References 16 publications

The Novel Cannabinoid CB1 Receptor Neutral Antagonist AM4113 Suppresses Food Intake and Food-Reinforced Behavior but Does not Induce Signs of Nausea in Rats

The Novel Cannabinoid CB1 Receptor Neutral Antagonist AM4113 Suppresses Food Intake and Food-Reinforced Behavior but Does not Induce Signs of Nausea in Rats

Affective neuroscience of pleasure: reward in humans and animals

Endocannabinoid Hedonic Hotspot for Sensory Pleasure: Anandamide in Nucleus Accumbens Shell Enhances ‘Liking’ of a Sweet Reward

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