Effects of Food Availability and Administration of Orexigenic and Anorectic Agents on Elevated Ethanol Drinking Associated With Drinking in the Dark Procedures

Lyons, Angela M.; Lowery, Emily G.; Sparta, Dennis R.; Thiele, Todd E.

doi:10.1111/j.1530-0277.2008.00784.x

Cited by 71 publications

(59 citation statements)

References 19 publications

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“…It seems likely that peripherally administered ghrelin will have similar effects on alcohol reward as we have previously shown that systemic ghrelin treatment also increases accumbal dopamine release, increases locomotor activity, and induces a CPP response (32). In contrast to our data for central ghrelin administration, another study did not observe a similar increase in alcohol consumption when ghrelin was administered peripherally (33). The most likely explanation for the discrepancy relates to the protocol.…”

Section: Discussioncontrasting

confidence: 55%

Requirement of central ghrelin signaling for alcohol reward

Jerlhag¹,

Egecioglu

Landgren³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

374

367

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The stomach-derived hormone ghrelin interacts with key CNS circuits regulating energy balance and body weight. Here we provide evidence that the central ghrelin signaling system is required for alcohol reward. Central ghrelin administration (to brain ventricles or to tegmental areas involved in reward) increased alcohol intake in a 2-bottle (alcohol/water) free choice limited access paradigm in mice. By contrast, central or peripheral administration of ghrelin receptor (GHS-R1A) antagonists suppressed alcohol intake in this model. Alcohol-induced locomotor stimulation, accumbal dopamine release and conditioned place preference were abolished in models of suppressed central ghrelin signaling: GHS-R1A knockout mice and mice treated with 2 different GHS-R1A antagonists. Thus, central ghrelin signaling, via GHS-R1A, not only stimulates the reward system, but is also required for stimulation of that system by alcohol. Our data suggest that central ghrelin signaling constitutes a potential target for treatment of alcohol-related disorders.appetite ͉ ethanol ͉ GHS-R1A ͉ mesolimbic dopamine system ͉ reinforcing

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Section: Discussioncontrasting

confidence: 55%

Requirement of central ghrelin signaling for alcohol reward

Jerlhag¹,

Egecioglu

Landgren³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

374

367

View full text Add to dashboard Cite

show abstract

“…Mice in each group were given access to either water or ethanol (20%), respectively, on a weekly schedule that started with 2 hours (2 h) access a day for 3 days, followed by 1 day 4 hour (4 h) access session, and then 3 days of abstinence, for a total of 6 weeks ( Figure 1a). Water and ethanol mice had similar body weights at the beginning and the end of the 6-week DID treatment (water: 20.5 ± 0.4 g and 24.7 ± 0.3 g; ethanol: 21.0 ±0.4 g and 24.7±0.3 g at week 1 and week 6, respectively; n ¼ 49-65), in agreement with previous results showing ethanol consumption during DID does not affect weight (Lyons et al, 2008).…”

Section: Resultssupporting

confidence: 81%

Erratum: Repeated Binge-Like Ethanol Drinking Alters Ethanol Drinking Patterns and Depresses Striatal GABAergic Transmission

Wilcox¹,

Carlson²,

Sherazee³

et al. 2014

Neuropsychopharmacol

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Repeated cycles of binge alcohol drinking and abstinence are key components in the development of dependence. However, the precise behavioral mechanisms underlying binge-like drinking and its consequences on striatal synaptic physiology remain unclear. In the present study, ethanol and water drinking patterns were recorded with high temporal resolution over 6 weeks of binge-like ethanol drinking using the 'drinking in the dark' (DID) protocol. The bottle exchange occurring at the beginning of each session prompted a transient increase in the drinking rate that might facilitate the acquisition of ethanol binge-like drinking. Ethanol drinking mice also displayed a 'front-loading' behavior, in which the highest rate of drinking was recorded during the first 15 min. This rate increased over weeks and paralleled the mild escalation of blood ethanol concentrations. GABAergic and glutamatergic transmission in the dorsal striatum were examined following DID. Spontaneous glutamatergic transmission and the density of dendritic spines were unchanged after ethanol drinking. However, the frequency of GABA A receptor-mediated inhibitory postsynaptic currents was depressed in medium spiny neurons of ethanol drinking mice. A history of ethanol drinking also increased ethanol preference and altered the acute ethanol effects on GABAergic transmission differentially in dorsolateral and dorsomedial striatum. Together, the study shows that the bottle exchange during DID promotes fast, voluntary ethanol drinking and that this intermittent pattern of ethanol drinking causes a depression of GABAergic transmission in the dorsal striatum.

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“…Similarly, DID does not rely on sucrose fading and does not appear to be a result of dietary demand, but does result in physical signs of intoxication. 65,66 Using the DID paradigm, TBI reduced overall intake at 17 days post-injury compared with that of sham controls.…”

Section: Discussionmentioning

confidence: 99%

Experimental Traumatic Brain Injury Alters Ethanol Consumption and Sensitivity

Lowing

Susick

Caruso

et al. 2014

Journal of Neurotrauma

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Altered alcohol consumption patterns after traumatic brain injury (TBI) can lead to significant impairments in TBI recovery. Few preclinical models have been used to examine alcohol use across distinct phases of the post-injury period, leaving mechanistic questions unanswered. To address this, the aim of this study was to describe the histological and behavioral outcomes of a noncontusive closed-head TBI in the mouse, after which sensitivity to and consumption of alcohol were quantified, in addition to dopaminergic signaling markers. We hypothesized that TBI would alter alcohol consumption patterns and related signal transduction pathways that were congruent to clinical observations. After midline impact to the skull, latency to right after injury, motor deficits, traumatic axonal injury, and reactive astrogliosis were evaluated in C57BL/6J mice. Amyloid precursor protein (APP) accumulation was observed in white matter tracts at 6, 24, and 72 h post-TBI. Increased intensity of glial fibrillary acidic protein (GFAP) immunoreactivity was observed by 24 h, primarily under the impact site and in the nucleus accumbens, a striatal subregion, as early as 72 h, persisting to 7 days, after TBI. At 14 days post-TBI, when mice were tested for ethanol sensitivity after acute high-dose ethanol (4 g/kg, intraperitoneally), brain-injured mice exhibited increased sedation time compared with uninjured mice, which was accompanied by deficits in striatal dopamine-and cAMP-regulated neuronal phosphoprotein, 32 kDa (DARPP-32) phosphorylation. At 17 days post-TBI, ethanol intake was assessed using the Drinking-in-the-Dark paradigm. Intake across 7 days of consumption was significantly reduced in TBI mice compared with sham controls, paralleling the reduction in alcohol consumption observed clinically in the initial post-injury period. These data demonstrate that TBI increases sensitivity to ethanol-induced sedation and affects downstream signaling mediators of striatal dopaminergic neurotransmission while altering ethanol consumption. Examining TBI effects on ethanol responsitivity will improve our understanding of alcohol use post-TBI in humans.

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Effects of Food Availability and Administration of Orexigenic and Anorectic Agents on Elevated Ethanol Drinking Associated With Drinking in the Dark Procedures

Cited by 71 publications

References 19 publications

Requirement of central ghrelin signaling for alcohol reward

Requirement of central ghrelin signaling for alcohol reward

Erratum: Repeated Binge-Like Ethanol Drinking Alters Ethanol Drinking Patterns and Depresses Striatal GABAergic Transmission

Experimental Traumatic Brain Injury Alters Ethanol Consumption and Sensitivity

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