Ghrelin amplifies the nicotine-induced dopamine release in the rat striatum

Palotai, Miklós; Bagosi, Zsolt; Jászberényi, Miklós; Csabafi, Krisztina; Dochnal, Roberta; Manczinger, Máté; Telegdy, Gyula; Szabó, Gyula

doi:10.1016/j.neuint.2013.06.014

Cited by 33 publications

(25 citation statements)

References 51 publications

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“…Our finding is supported by a recent study which found that mecamylamine decreased pavlovian incentive motivation for sugar (Ostlund et al, 2014) and operant self-administration, albeit at much higher doses (Ford et al, 2009). Further, an in vitro application of mecamylamine in the NAc, decreased ghrelin-mediated accumbal DA release (Palotai et al, 2013). Cytisine, a β2 selective nAChR agonist, marketed as a smoking cessation aid Tabex in eastern European countries, also reduced sucrose consumption.…”

Section: Discussionsupporting

confidence: 88%

“…In yet another study, in vitro application of mecamylamine at the level of the NAc, decreased ghrelin-mediated accumbal DA release (Palotai et al, 2013), corroborating the role of mecamylamine at the level of NAc.…”

Section: Chapter 5: General Discussionsupporting

confidence: 53%

“…Interestingly, a recent study found that the in vitro application of the nAChR non-selective non-competitive antagonist mecamylamine, decreased ghrelin-mediated rat accumbal DA release (Palotai et al, 2013). Indeed, various data in rodent models point to the direct interaction of ghrelin with the cholinergic-DAergic reward link, albeit in the VTA (Egecioglu et al, 2010, Dickson et al, 2011.…”

Section: Dopamine and The Nachr In The Nac -Mediating Reward-related Bementioning

confidence: 99%

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The Effects of Binge-Like Sucrose Consumption on the Mesolimbic Reward Pathway in the Brain

Shariff¹

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Obesity is becoming a worldwide epidemic (WHO, 2000, Leigh and Morris, 2016, Lifshitz and Lifshitz, 2014, James, 2004. Pharmacotherapeutics that attempt to stem overweight and obesity have largely been ineffective and often are accompanied by adverse side effects (Glazer, 2001). It is therefore imperative to develop effective strategies to combat obesity. A paradigm that has gained momentum relatively recently is the development of addiction to fat and sweet food (Fortuna, 2012, Smith and Robbins, 2013, Volkow et al., 2013a. While drugs of abuse affect various brain subregions, they have been shown to act on three major areas of the brain, namely the brain stem, the limbic system and the cerebral cortex (NIDA, 2010).The limbic system is an interconnected collection of brain structures such as the nucleus accumbens (NAc) and the basolateral amygdala (BLA), whose neural connectivities encode emotional states such as anticipation of reward and motivation (Berridge, 2012). At the molecular level, in addition to the various dysregulatory outcomes in relation to neurotransmitters, it is the dysregulation of balance between dopamine (DA) and acetylcholine (ACh) in the limbic system, especially in the NAc that has been found to drive and maintain behaviours that perpetuate addiction to substances of abuse (Hoebel et al., 2007, Aosaki et al., 2010. Interestingly, sucrose, a potent contributor to the development of obesity (Lakhan and Kirchgessner, 2013, Tappy et al., 2010), has been shown, albeit indirectly, to affect the release of DA in the NAc via the nAChRs (Avena et al., 2008). The role of specific subtypes of nAChRs in the NAc has yet to be elucidated in relation to sucrose consumption.Firstly, this study establishes that the nAChRs are involved in regulating sucrose consumption. Based on the various nAChRs agonists/partial agonists and antagonists tested systemically, it is surmised that *nAChRs are involved in mediating sucrose consumption.Furthermore, coupled to the changes in nAChRs, this study also sheds light for the first time ii on the global morphological changes that occur in the dendrites of the neurons in the NAc and BLA reminiscent of similar changes due to drugs of abuse, suggestive of a global imbalance at the level of the NAc and amygdala. Further studies are warranted to determine the precise functional significance of the morphological changes that are reported in this study, and to discover potential newer pharmacotherapies that target the nAChRs. At the present time, however, varenicline, an FDA approved pharmacotherapeutic, appears to be an attractive agent in reducing sucrose intake. Varenicline may hold potential benefits in lowering weight gain thus concomitantly lowering the global burden of obesity-related disease.iii

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Section: Discussionsupporting

confidence: 88%

Section: Chapter 5: General Discussionsupporting

confidence: 53%

Section: Dopamine and The Nachr In The Nac -Mediating Reward-related Bementioning

confidence: 99%

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The Effects of Binge-Like Sucrose Consumption on the Mesolimbic Reward Pathway in the Brain

Shariff¹

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“…Ghrelin also declines following two months of successful abstinence from nicotine (Lee, Joe et al 2006) but some have shown that ghrelin is not associated nicotine craving and withdrawal symptoms (Mutschler et al, 2012). In addition, ghrelin interacts with the nicotinic acetylcholine receptor to stimulate dopamine release in the brain, particularly in areas related to drug reward and emotional functioning (Jerlhag, Janson, Waters, & Engel, 2012; Palotai et al, 2013a, 2013b). An early genetic study has identified ghrelin genes and personality trait relationships that may have implications for trait differences between alcoholics and non-alcoholics (Landgren et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Peptide YY and ghrelin predict craving and risk for relapse in abstinent smokers

Al’Absi

Lemieux

Nakajima

2014

Psychoneuroendocrinology

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Appetite hormones are directly involved in regulating satiety, energy expenditure, and food intake, and accumulating evidence suggests their involvement in regulating reward and craving for drugs. This study investigated the ability of peptide YY (PYY) and ghrelin during the initial 24–48 hours of a smoking cessation attempt to predict smoking relapse at 4 weeks. Multiple regression analysis indicated that increased PYY was associated with decreased reported craving and increased positive affect. Cox proportional hazard models showed that higher ghrelin levels predicted increased risk of smoking relapse (Hazard Ratio=2.06, 95% CI=1.30 – 3.27). These results indicate that circulating PYY may have buffering effects during the early stages of cessation while ghrelin may confer increased risk of smoking relapse. Further investigation of the links between these hormones and nicotine dependence is warranted.

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“…Exposure to nicotine not only targets nACh receptors throughout the brain but may lead to a release of dopamine including those from the VTA. The dopamine release by nicotine in the striatum of rats is facilitated by ghrelin − a growth hormone releasing peptide [111] . Ghrelin may also independently trigger the DA release.…”

Section: Nicotinementioning

confidence: 99%

Addictive neurons

2018

Ther Targets Neurol Dis

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Since the reward center is considered to be the area tegmentalis ventralis of the hypothalamus, logically its neurons could mainly be responsible for addiction. However, the literature asserts that almost any neurons of CNS can respond to one or another addictive compound. Obviously not only addictive nicotine, but also alcohol, amphetamine, cannabis, cocaine, heroin and morphine may influence dopaminergic cells alone in VTA. Moreover, paradoxically some of these drugs ameliorate symptoms, counterbalance syndromes, cure diseases and improve health, not only those related to the CNS and in adults, but also almost all other organs and in children, e.g. epilepsy.

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Ghrelin amplifies the nicotine-induced dopamine release in the rat striatum

Cited by 33 publications

References 51 publications

The Effects of Binge-Like Sucrose Consumption on the Mesolimbic Reward Pathway in the Brain

The Effects of Binge-Like Sucrose Consumption on the Mesolimbic Reward Pathway in the Brain

Peptide YY and ghrelin predict craving and risk for relapse in abstinent smokers

Addictive neurons

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