Cholecystokinin reduces ethanol consumption in golden hamsters

DiBattista, David; McKenzie, Tammy L. B.; Hollis-walker, Laurie

doi:10.1016/s0741-8329(03)00036-3

Cited by 11 publications

(2 citation statements)

References 34 publications

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“…Previous studies indicate that, for example, melanocortins and cholecystokinin can also reduce alcohol intake e.g. [31], [32]. Notably both peptides have previously been shown to interact with GLP-1.…”

Section: Discussionmentioning

confidence: 97%

Gut Peptide GLP-1 and Its Analogue, Exendin-4, Decrease Alcohol Intake and Reward

2013

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Glucagon-like-peptide-1 (GLP-1) is a gut- and neuro-peptide with an important role in the regulation of food intake and glucose metabolism. Interestingly, GLP-1 receptors (GLP-1R) are expressed in key mesolimbic reward areas (including the ventral tegmental area, VTA), innervated by hindbrain GLP-1 neurons. Recently GLP-1 has emerged as a potential regulator of food reward behavior, an effect driven by the mesolimbic GLP-1Rs. Its role in other reward behaviors remains largely unexplored. Since a considerable overlap has been suggested for circuitry controlling reward behavior derived from food and alcohol we hypothesized that GLP-1 and GLP-1Rs could regulate alcohol intake and alcohol reward. We sought to determine whether GLP-1 or its clinically safe stable analogue, Exendin-4, reduce alcohol intake and reward. To determine the potential role of the endogenous GLP-1 in alcohol intake we evaluated whether GLP-1R antagonist, Exendin 9-39, can increase alcohol intake. Furthermore, we set out to evaluate whether VTA GLP-1R activation is sufficient to reduce alcohol intake. Male Wistar rats injected peripherally with GLP-1 or Exendin-4 reduced their alcohol intake in an intermittent access two bottle free choice drinking model. Importantly, a contribution of endogenously released GLP-1 is highlighted by our observation that blockade of GLP-1 receptors alone resulted in an increased alcohol intake. Furthermore, GLP-1 injection reduced alcohol reward in the alcohol conditioned place preference test in mice. To evaluate the neuroanatomical substrate linking GLP-1 with alcohol intake/reward, we selectively microinjected GLP-1 or Exendin 4 into the VTA. This direct stimulation of the VTA GLP-1 receptors potently reduced alcohol intake. Our findings implicate GLP-1R signaling as a novel modulator of alcohol intake and reward. We show for the first time that VTA GLP-1R stimulation leads to reduced alcohol intake. Considering that GLP-1 analogues are already approved for clinical use, this places the GLP system as an exciting new potential therapeutic target for alcohol use disorders.

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Section: Discussionmentioning

confidence: 97%

Gut Peptide GLP-1 and Its Analogue, Exendin-4, Decrease Alcohol Intake and Reward

2013

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“…Furthermore, there are examples of overlapping control of feeding and ethanol intake by other neurochemical systems Thiele et al, 2004). It has been known for some time that the peptide cholecystokinin reduces food intake and ethanol consumption in a dosedependent fashion (Avery and Livosky, 1986;DiBattista et al, 2003;Kulkosky and Chavez, 1984;Kulkosky et al, 1991;Kulkosky and Glazner, 1988;Le Sauter et al, 1988), and recent evidence shows that the orexigenic neuropeptide galanin (Kyrkouli et al, 1990;Tempel et al, 1988) controls ethanol consumption (Leibowitz et al, 2003;Lewis et al, 2004). A growing body of literature also shows that the central cannabinoid system modulates ethanol selfadministration and feeding (Colombo et al, 1998;Freedland et al, 2003;Poncelet et al, 2003;Wang et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Effects of Melanocortin Receptor Activation and Blockade on Ethanol Intake: A Possible Role for the Melanocortin-4 Receptor

Navarro

Cubero

Chen

et al. 2005

Alcoholism: Clinical & Experimental Research

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Background-The melanocortin (MC) system is composed of peptides that are cleaved from the polypeptide precursor proopiomelanocortin. A growing body of literature suggests that the MC system modulates neurobiological responses to drugs of abuse. Because ethanol has direct effects on central proopiomelanocortin activity, it is possible that MC neuropeptides participate in the control of voluntary ethanol consumption. Here we assessed the possibility that MC receptor (MCR) agonists modulate ethanol intake via the MC3 receptor (MC3R) and/or the MC4 receptor (MC4R) and whether the MCR antagonist AgRP-(83-132) controls ethanol consumption.

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