Augmentation of drug reward by chronic food restriction

Carr, Kenneth D

doi:10.1016/s0031-9384(02)00759-x

Cited by 300Neurotransmitter Receptor Influence on BehaviorRegulation of Appetite and ObesityNeuroscience and Neuropharmacology Research

Augmentation of drug reward by chronic food restriction

Carr, Kenneth D·2002·Physiology & Behavior

DOI 10.1016/s0031-9384(02)00759-x

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Abstract

Chronic food restriction and maintenance of low body weight have long been known to increase the self-administration and motor-activating effects of abused drugs. Using a lateral hypothalamic self-stimulation (LHSS) rate-frequency method, it is shown that chronic food restriction augments the rewarding (i.e., threshold lowering) effect of diverse drugs of abuse. Further, the effect is attributed to increased sensitivity of a neural substrate, rather than a change in drug bioavailability or pharmacokinetics, because it is preserved when drugs are injected directly into the lateral cerebral ventricle (intracerebroventricularly). The food restriction regimen that augments drug reward also increases the induction of c-fos, by intracerebroventricular amphetamine, in limbic forebrain dopamine (DA) terminal areas. The possibility of increased DA receptor function is suggested by findings that rewarding and motor-activating effects of direct DA receptor agonists are augmented by food restriction, and the augmented behavioral effects of amphetamine are reversed by an otherwise subthreshold dose of D-1 antagonist. Initial studies of DA receptor-mediated signal transduction, that are focused on the D-2 receptor, suggest increased functional coupling between receptor and G-protein (i.e., quinpirole-stimulated [(35)S]GTPgammaS binding) in dorsal striatum. Unlike behavioral sensitization induced by intermittent stress or psychostimulant treatment, which persist indefinitely following induction, the augmenting effect of food restriction abates within 1 week of restored ad libitum feeding and weight gain. The possible involvement of endocrine hormones and/or 'feeding-related' neuropeptides, whose levels change dynamically with depletion and repletion of adipose stores, is therefore under investigation. Initial tests have been limited to acute treatments aimed at attenuating the effects of hypoinsulinemia, hypoleptinemia and elevated corticosterone levels in food-restricted rats. None of these treatments has attenuated the behavioral effect of food restriction. While a melanocortin receptor agonist has been found to enhance drug reward, melanocortin receptors do not seem to mediate the augmenting effect of food restriction. Continuing investigations of endocrine adiposity signals, 'feeding-related' neuropeptides and dopaminergic signal transduction may further elucidate the way in which drugs of abuse exploit mechanisms that mediate survival-related behavior, and help explain the high comorbidity of drug abuse and eating disorders.

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Carr (2002) suggested that food-restriction sensitizes the meso-limbic dopamine system.
“Indeed, Carr (2002) suggested that food-restriction “sensitizes” the meso-limbic dopamine system.”
From Dopamine reward circuitry: Two projection systems from the ventral midbrain to the nucleus accumbens–olfactory tubercle complex (2007) · cites this paper as Carr, 2002

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Authors: Carr, K. D.
Affiliations: New York University (US)
Corresponding author: Carr, Kenneth D
ORCID: Carr, Kenneth D
Venue: Physiology & Behavior
Publisher: Elsevier BV
Published: 2002-07
Volume: 76
Issue: 3
Pages: 353-364
ISSN: 0031-9384 (ISSN-L)
DOI: 10.1016/s0031-9384(02)00759-x
OpenAlex: W122691953
Cited by: 300
References: 127
Citations by year: 2026: 3 · 2025: 6 · 2024: 7 · 2023: 8 · 2022: 6 · 2021: 11 · 2020: 9 · 2019: 9 · 2018: 6 · 2017: 8 · 2016: 5 · 2015: 12 · 2014: 14 · 2013: 16 · 2012: 17
FWCI: 6.10
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Physiology & Behavior (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute on Drug Abuse (R01DA003956, K02DA000292, KO2-DA00292)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: chronic food restriction, drug reward, dopamine receptor signaling, c-fos induction, amphetamine, dopamine D2 receptor, G protein coupling, melanocortin receptors, hypoleptinemia, hypoinsulinemia, corticosterone, behavioral sensitization
MeSH terms: Animals, Behavior, Behavior, Animal, Brain Chemistry, Food Deprivation, Hormones, Humans, Neuropeptides, Reward, Neurotransmitter Agents, Opioid Peptides, Substance-Related Disorders, Rats

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Augmentation of drug reward by chronic food restriction

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