A role for leptin and ghrelin in the augmentation of heroin seeking induced by chronic food restriction

D'Cunha, Tracey; Chisholm, Alexandra; Hryhorczuk, Cécile; Fulton, Stephanie; Shalev, Uri

doi:10.1007/s00213-019-05415-9

Cited by 19 publications

(9 citation statements)

References 53 publications

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“…administration of the GHS-R1A antagonist, D-Lys-3-GHRP-6 had no effect on ongoing heroin self-administration under a fixed-ratio 1 schedule (FR1), or on the food deprivation-induced reinstatement of heroin seeking [ 203 ]. Nevertheless, recent experiment of the same research group, wherein JMV2959 was microinjected into the VTA, showed that the GHS-R1A antagonism dose-dependently decreased heroin seeking in the food-restricted rats [ 204 ], which confirmed the similar JMV2959 effects published previously elsewhere (see below).…”

Section: Ghrelin/ghs-r1a and Opioidssupporting

confidence: 83%

The Role of Ghrelin/GHS-R1A Signaling in Nonalcohol Drug Addictions

Sustkova-Fiserova

Charalambous

Khryakova

et al. 2022

IJMS

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Drug addiction causes constant serious health, social, and economic burden within the human society. The current drug dependence pharmacotherapies, particularly relapse prevention, remain limited, unsatisfactory, unreliable for opioids and tobacco, and even symptomatic for stimulants and cannabinoids, thus, new more effective treatment strategies are researched. The antagonism of the growth hormone secretagogue receptor type A (GHS-R1A) has been recently proposed as a novel alcohol addiction treatment strategy, and it has been intensively studied in experimental models of other addictive drugs, such as nicotine, stimulants, opioids and cannabinoids. The role of ghrelin signaling in these drugs effects has also been investigated. The present review aims to provide a comprehensive overview of preclinical and clinical studies focused on ghrelin’s/GHS-R1A possible involvement in these nonalcohol addictive drugs reinforcing effects and addiction. Although the investigation is still in its early stage, majority of the existing reviewed experimental results from rodents with the addition of few human studies, that searched correlations between the genetic variations of the ghrelin signaling or the ghrelin blood content with the addictive drugs effects, have indicated the importance of the ghrelin’s/GHS-R1As involvement in the nonalcohol abused drugs pro-addictive effects. Further research is necessary to elucidate the exact involved mechanisms and to verify the future potential utilization and safety of the GHS-R1A antagonism use for these drug addiction therapies, particularly for reducing the risk of relapse.

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Section: Ghrelin/ghs-r1a and Opioidssupporting

confidence: 83%

The Role of Ghrelin/GHS-R1A Signaling in Nonalcohol Drug Addictions

Sustkova-Fiserova

Charalambous

Khryakova

et al. 2022

IJMS

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“…Chronic food restriction as well as acute food deprivation have both been found to reinstate drug reward associations and drug seeking behavior [90] [91]. Interestingly, chronic food restriction appears to induce relapse via different Accepted Article mechanisms than acute food deprivation [92]. Reinstatement of heroin seeking by acute food deprivation appears to rely on corticotropin releasing factor (CRF) signaling [93], as well as dopamine D1 receptor signaling [94,95].…”

Section: Hunger Triggers Reinstatement Of Drug Seekingmentioning

confidence: 99%

Hunger‐driven adaptive prioritization of behavior

Smith

Grueter

2021

The FEBS Journal

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In order to survive, an animal must adapt its behavioral priorities to accommodate changing internal and external conditions. Hunger, a universally recognized interoceptive signal, promotes food intake though increasingly well understood neural circuits. Less understood, is how hunger is integrated into the neural computations that guide non-feeding behaviors. Within the brain, agoutirelated peptide (AGRP) neurons in the arcuate nucleus of the hypothalamus have been found to powerfully stimulate feeding in addition to mediating other hunger-driven behavioral phenotypes. In this review, we compile the behavioral plasticity downstream of hunger, and present identified or potential molecular and neural circuit mechanisms. We catalogue hunger's ability to increase exploration, decrease anxiety, and alter social behavior, among other phenotypes. Finally, we suggest paths forward for understanding hunger-driven behavioral adaptation and discuss the benefits of understanding state-dependent modulation of neural circuits controlling behavior. Hunger biases behavior toward feeding Animals engage in a wide range of behaviors to fulfill goals critical to life and reproduction. In order to thrive, an animal must appropriately prioritize the behaviors that address their most pertinent needs. The need for food represents one of nature's most fundamental obligations. Hunger, the interoceptive reporter of energy deficit, is a universally recognized signal that triggers a pervasive shift in behavior (Fig. 1). The hungry animal must engage in a significantly altered behavioral complement relative to the fed animal to fulfill this need. Disruption in this complex interaction between energy level and behavior, leading to an abnormal behavioral response to energy deficit or

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“…We also observed a robust increase in heroin seeking in chronically food-restricted rats following a withdrawal period (D'Cunha et al, 2013;Sedki et al, 2013). More recently, we have demonstrated a critical role for the metabolic hormones ghrelin and leptin in the ventral tegmental area (D'Cunha et al, 2020), and for dopamine transmission in the nucleus accumbens (NAc) in food restriction-induced augmentation of heroin seeking (D'Cunha et al, 2017). However, the neural circuitry that underlies the impact of food restriction on drug seeking has not been entirely elucidated.…”

Section: Introductionmentioning

confidence: 96%

Assessing the Role of Corticothalamic and Thalamo-Accumbens Projections in the Augmentation of Heroin Seeking in Chronically Food-Restricted Rats

et al. 2020

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Drug addiction is a chronic disorder characterized by compulsive drug seeking, and involves repetitive cycles of compulsive drug use, abstinence, and relapse. In both human and animal models of addiction, chronic food restriction increases rates of relapse. Our laboratory has reported a robust increase in drug seeking following a period of withdrawal in chronically foodrestricted rats compared with sated controls. Recently, we reported that activation of the paraventricular nucleus of the thalamus (PVT) abolished heroin seeking in chronically food-restricted rats. However, the precise inputs and outputs of the PVT that mediate this effect remain elusive. The goal of the current study was to determine the role of corticothalamic and thalamo-accumbens projections in the augmentation of heroin seeking induced by chronic food restriction. Male Long-Evans rats were trained to self-administer heroin for 10 d. Next, rats were removed from the self-administration chambers and were subjected to a 14 d withdrawal period while sated (unlimited access to food) or mildly food-restricted (FDR). On day 14, rats were returned to the self-administration context for a 3 h heroin-seeking test under extinction conditions during which corticothalamic and thalamo-accumbens neural activity was altered using chemogenetics. Surprisingly, chemogenetic activation or inhibition of corticothalamic projections did not alter heroin-seeking behavior. Chemogenetic activation of thalamo-accumbens shell, but not core, projectors attenuated heroin seeking in FDR rats. The results indicate an important role for the PVT to nucleus accumbens shell projections in the augmentation of heroin seeking induced by chronic food restriction.

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A role for leptin and ghrelin in the augmentation of heroin seeking induced by chronic food restriction

Cited by 19 publications

References 53 publications

The Role of Ghrelin/GHS-R1A Signaling in Nonalcohol Drug Addictions

The Role of Ghrelin/GHS-R1A Signaling in Nonalcohol Drug Addictions

Hunger‐driven adaptive prioritization of behavior

Assessing the Role of Corticothalamic and Thalamo-Accumbens Projections in the Augmentation of Heroin Seeking in Chronically Food-Restricted Rats

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