The area postrema (AP) and the parabrachial nucleus (PBN) are important sites for salmon calcitonin (sCT) to decrease evoked phasic dopamine release in the nucleus accumbens (NAc)

Whiting, Lynda; McCutcheon, James E.; Boyle, Christina N.; Roitman, Mitchell F.; Lutz, Thomas

doi:10.1016/j.physbeh.2017.03.023

Cited by 25 publications

(18 citation statements)

References 50 publications

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“…Although there is no robust evidence that sCT crosses the blood-brain barrier effectively, there are data showing that peripheral sCT did not affect food intake in rats with a knocked down calcitonin receptor in the VTA but decreased food intake in control (Mietlicki-Baase et al 2015b). Moreover, a recent study showed that peripherally administered sCT decreased VTA-evoked phasic dopamine release in the NAc (Whiting et al 2017), supporting our notion that sCT acts centrally on the mesolimbic dopamine system to regulate dopamine neurotransmission. In line with the present results, we therefore suggest that sCT crosses the blood-brain barrier and reaches areas of the midbrain to regulate alcohol reinforcement.…”

Section: Discussionsupporting

confidence: 69%

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

2018

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Alcohol expresses its reinforcing properties by activating areas of the mesolimbic dopamine system, which consists of dopaminergic neurons projecting from the ventral tegmental area to the nucleus accumbens. The findings that reward induced by food and addictive drugs involve common mechanisms raise the possibility that gut-brain hormones, which control appetite, such as amylin, could be involved in reward regulation. Amylin decreases food intake, and despite its implication in the regulation of natural rewards, tenuous evidence support amylinergic mediation of artificial rewards, such as alcohol. Therefore, the present experiments were designed to investigate the effect of salmon calcitonin (sCT), an amylin receptor agonist and analogue of endogenous amylin, on various alcohol-related behaviours in rodents. We showed that acute sCT administration attenuated the established effects of alcohol on the mesolimbic dopamine system, particularly alcohol-induced locomotor stimulation and accumbal dopamine release. Using the conditioned place preference model, we demonstrated that repeated sCT administration prevented the expression of alcohol's rewarding properties and that acute sCT administration blocked the reward-dependent memory consolidation. In addition, sCT pre-treatment attenuated alcohol intake in low alcohol-consuming rats, with a more evident decrease in high alcohol consumers in the intermittent alcohol access model. Lastly, sCT did not alter peanut butter intake, blood alcohol concentration and plasma corticosterone levels in mice. Taken together, the present data support that amylin signalling is involved in the expression of alcohol reinforcement and that amylin receptor agonists could be considered for the treatment of alcohol use disorder in humans.

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Section: Discussionsupporting

confidence: 69%

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

2018

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“…These data suggest that, besides direct homeostatic signaling to mesolimbic circuitry, these signals can be initially gated by hindbrain processes before being relayed to the mesolimbic circuits. Further support for this hypothesis can be observed in animals with lesions to the area postrema (AP) and parabrachial nucleus (PBN) - while amylin receptor activation can reduce VTA stimulated dopamine release in the NAc in control animals, these effects are abolished in animals with either AP or PBN lesions ( 152 ).…”

Section: Neuronal Inputs To Mesolimbic Pathways That Regulate Homeostmentioning

confidence: 96%

“…Moreover, NAc core D1/D2 dopamine receptor activation partially rescues the food intake suppressive effects of VTA amylin receptor activation ( 151 ). It remains possible, though, that some of the effects of amylin may be either indirect, through action in the area postrema or via the calcitonin receptor ( 152 ). VTA amylin signaling also synergistically acts with leptin receptor signaling, where combined activation of receptors for these hormones in the VTA produces weight loss and hypophagia ( 153 ).…”

Section: Homeostatic Signals Are Relayed To Mesolimbic Pathwaysmentioning

confidence: 99%

Parallels and Overlap: The Integration of Homeostatic Signals by Mesolimbic Dopamine Neurons

2018

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Motivated behaviors are often initiated in response to perturbations of homeostasis. Indeed, animals and humans have fundamental drives to procure (appetitive behaviors) and eventually ingest (consummatory behaviors) substances based on deficits in body fluid (e.g., thirst) and energy balance (e.g., hunger). Consumption, in turn, reinforces motivated behavior and is therefore considered rewarding. Over the years, the constructs of homeostatic (within the purview of the hypothalamus) and reward (within the purview of mesolimbic circuitry) have been used to describe need-based vs. need-free consumption. However, many experiments have demonstrated that mesolimbic circuits and “higher-order” brain regions are also profoundly influenced by changes to physiological state, which in turn generate behaviors that are poised to maintain homeostasis. Mesolimbic pathways, particularly dopamine neurons of the ventral tegmental area (VTA) and their projections to nucleus accumbens (NAc), can be robustly modulated by a variety of energy balance signals, including post-ingestive feedback relaying nutrient content and hormonal signals reflecting hunger and satiety. Moreover, physiological states can also impact VTA-NAc responses to non-nutritive rewards, such as drugs of abuse. Coupled with recent evidence showing hypothalamic structures are modulated in anticipation of replenished need, classic boundaries between circuits that convey perturbations in homeostasis and those that drive motivated behavior are being questioned. In the current review, we examine data that have revealed the importance of mesolimbic dopamine neurons and their downstream pathways as a dynamic neurobiological mechanism that provides an interface between physiological state, perturbations to homeostasis, and reward-seeking behaviors.

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“…The caudal hindbrain area postrema (AP) and nucleus of the solitary tract (NTS) are critically involved in mediating the effects of amylin on eating [9] . However, recent data indicate that other areas of the brain, including the hypothalamic arcuate (ARC) or ventromedial (VMN) nucleus [10] , [11] , ventral tegmental area (VTA) [12] , [13] , and lateral dorsal tegmental nucleus (LDTg) [14] , may be directly or indirectly targeted by amylin to influence hedonic aspects of eating such as reward-guided behaviors that may contribute to the food selection [15] , [16] . This review will briefly summarize amylin physiology and pharmacology and then focus on the amylin's role in food reward and the effects of amylin analogs in pre-clinical testing for anti-obesity drugs.…”

Section: Amylin In the Control Of Energy Metabolismmentioning

confidence: 99%

Amylin – Its role in the homeostatic and hedonic control of eating and recent developments of amylin analogs to treat obesity

Boyle

Lutz

Foll

2018

Molecular Metabolism

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BackgroundAmylin is a pancreatic β-cell hormone that produces effects in several different organ systems. One of its best-characterized effects is the reduction in eating and body weight seen in preclinical and clinical studies. Amylin activates specific receptors, a portion of which it shares with calcitonin gene-related peptide (CGRP). Amylin's role in the control of energy metabolism relates to its satiating effect, but recent data indicate that amylin may also affect hedonic aspects in the control of eating, including a reduction of the rewarding value of food. Recently, several amylin-based peptides have been characterized. Pramlintide (Symlin®) is currently the only one being used clinically to treat type 1 and type 2 diabetes. However other amylin analogs with improved pharmacokinetic properties are being considered as anti-obesity treatment strategies. Several other studies in obesity have shown that amylin agonists could also be useful for weight loss, especially in combination with other agents.Scope of reviewThis review will briefly summarize amylin physiology and pharmacology and then focus on amylin's role in food reward and the effects of amylin analogs in pre-clinical testing for anti-obesity drugs.ConclusionWe propose here that the effects of amylin may be homeostatic and hedonic in nature.

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The area postrema (AP) and the parabrachial nucleus (PBN) are important sites for salmon calcitonin (sCT) to decrease evoked phasic dopamine release in the nucleus accumbens (NAc)

Cited by 25 publications

References 50 publications

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

Activation of amylin receptors attenuates alcohol‐mediated behaviours in rodents

Parallels and Overlap: The Integration of Homeostatic Signals by Mesolimbic Dopamine Neurons

Amylin – Its role in the homeostatic and hedonic control of eating and recent developments of amylin analogs to treat obesity

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