Responding for brain stimulation reward in the bed nucleus of the stria terminalis in alcohol‐preferring rats following alcohol and amphetamine pretreatments

Eiler, William J.A.; Hardy, Lathen; Goergen, Josuha; Seyoum, Regat; Mensah-Zoe, Boikai; June, Harry L.

doi:10.1002/syn.20437

Cited by 12 publications

(17 citation statements)

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“…This interpretation is based on a model of reward perception in which the effects of alcohol and electrical brain stimulation on mesocorticolimbic activity sum to increase the total amount of positive reinforcement experienced as the mice respond for a given stimulation frequency. This finding replicates earlier studies in rats, where alcohol administration directly lowered BSR thresholds (Eiler et al, 2007; Lewis and June, 1994; Moolten and Kornetsky, 1990) and is consistent with chronic exposure studies that find elevated BSR thresholds upon the removal of alcohol from dependent rats (Rylkova et al, 2008; Schulteis et al, 1995). In the current study, 0.6 g/kg alcohol lowered BSR threshold by approximately 20% in both C57 and DBA mice, an effect that occurred in the first 15 minutes after administration and was not significant in either strain at later time points.…”

Section: Discussionsupporting

confidence: 91%

“…Early studies (e.g., Vrtunski et al, 1973) relied solely on maximal response rates as the behavioral index of reward and suggested that alcohol can increase responding for BSR. More recent studies reveal that self- or experimenter-administered alcohol can lower BSR thresholds without changing response rates, indicating a potentiation of brain reward circuitry (Eiler et al, 2007; Lewis and June, 1994; Moolten and Kornetsky, 1990). Others have found increases or no effect on stimulation thresholds (Carlson and Lydic, 1976; Ghosh et al, 1991; Schaefer and Michael, 1987).…”

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confidence: 99%

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Alcohol, Cocaine, and Brain Stimulation‐Reward in C57Bl6/J and DBA2/J Mice

Fish

Riday

McGuigan

et al. 2009

Alcoholism Clin & Exp Res

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Background Pleasure and reward are critical features of alcohol drinking that are difficult to measure in animal studies. Intracranial self-stimulation (ICSS) is a behavioral method for studying the effects of drugs directly on the neural circuitry that underlies brain reward. These experiments had 2 objectives: first, to establish the effects of alcohol on ICSS responding in the C57Bl6/J (C57) and DBA2/J (DBA) mouse strains; and second, to compare these effects to those of the psychostimulant cocaine. Methods Male C57 and DBA mice were implanted with unipolar stimulating electrodes in the lateral hypothalamus and conditioned to spin a wheel for reinforcement by the delivery of rewarding electrical stimulation (i.e., brain stimulation-reward or BSR). Using the curve-shift method, the BSR threshold (θ0) was determined immediately before and after oral gavage with alcohol (0.3, 0.6, 1.0, 1.7 g/kg) or water. Blood alcohol concentration (BAC) was measured to determine the influence of alcohol metabolism on BSR threshold. Separately, mice were administered cocaine (1.0, 3.0, 10.0, 30.0 mg/kg) or saline intraperitoneally. Results In C57 mice, the 0.6 g/kg dose of alcohol lowered BSR thresholds by about 20%, during the rising (up to 40 mg/dl), but not falling, phase of BAC. When given to the DBA mice, alcohol lowered BSR thresholds over the entire dose range; the largest reduction was by about 50%. Cocaine lowered BSR thresholds in both strains. However, cocaine was more potent in DBA mice than in C57 mice as revealed by a leftward shift in the cocaine dose–response curve. For both alcohol and cocaine, effects on BSR threshold were dissociable from effects on operant response rates. Conclusions In C57 and DBA mice, reductions in BSR threshold reflect the ability of alcohol to potentiate the neural mechanisms of brain reward. The DBA mice are more sensitive to the reward-potentiating effects of both alcohol and cocaine, suggesting that there are mouse strain differences in the neural mechanisms of brain reward that can be measured with the ICSS technique.

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

Alcohol, Cocaine, and Brain Stimulation‐Reward in C57Bl6/J and DBA2/J Mice

Fish

Riday

McGuigan

et al. 2009

Alcoholism Clin & Exp Res

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“…Additionally, while the group mean data revealed no significant differences in the reward-enhancing effects of ethanol, exploratory analyses suggested that adolescent intermittent ethanol exposure may perhaps also increase sensitivity to the rewarding or appetitive effects of ethanol. Rodents selectively bred for high ethanol consumption show similar ethanol sensitivities (Chester et al, 2006; Eiler et al, 2007; Fish et al, 2012), suggesting that high sensitivity to ethanol reward and low sensitivity to ethanol withdrawal may predict heavy or problematic alcohol use.…”

Section: Discussionmentioning

confidence: 99%

“…However, the long-term effects of adolescent ethanol exposure on brain reward function during re-exposure to ethanol in adulthood have not been studied. Interestingly, rodent strains bred for high ethanol consumption exhibit heightened sensitivity to the reward-enhancing effects of ethanol and blunted sensitivity to the anhedonia associated with ethanol withdrawal (Chester et al, 2006; Eiler et al, 2007; Fish et al, 2012). These findings suggest that heightened sensitivity to the reward-enhancing effects of ethanol or blunted sensitivity to the anhedonia of ethanol withdrawal accompany and may predict increased ethanol consumption.…”

Section: Introductionmentioning

confidence: 99%

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Boutros

Semenova

Markou

2014

European Neuropsychopharmacology

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Adolescent alcohol use may interfere with neurodevelopment, increasing the likelihood of adult alcohol use disorders (AUDs). We investigated whether adolescent intermittent ethanol (AIE) exposure alters the adult reward response to ethanol. Adolescent rats were administered ethanol once (moderate exposure; Cohort 1) or three times per day (severe exposure; Cohort 2) in a 2 days on/2 days off pattern. In adulthood, subjects responded for electrical stimulation directed at the posterior lateral hypothalamus in a discrete-trials intracranial self-stimulation (ICSS) procedure that provides current-intensity thresholds as a measure of brain reward function. The effects of ethanol administration and withdrawal were assessed. Control rats showed dose-dependent threshold elevations after acute ethanol, indicating reward deficits. A majority of moderately AIE-exposed rats (Cohort 1) showed threshold lowering after ethanol, suggesting ethanol-induced reward enhancement in this sub-set of rats. Rats exposed to severe AIE (Cohort 2) showed no threshold elevation or lowering, suggesting blunted affective ethanol response. Daily ethanol induced threshold elevations 24 h after administration in control but not in either group of AIE-exposed rats, suggesting decreased sensitivity to the negative affective state of ethanol withdrawal. Withdrawal from a 4-day ethanol binge produced robust and enduring threshold elevations in all rats, although threshold elevations were diminished in rats exposed to severe AIE. These results indicate that AIE exposure diminished reward deficits associated with ethanol intoxication and withdrawal and may have increased ethanol-induced reward enhancement in a sub-set of rats. In humans, enhanced ethanol reward accompanied by reduced withdrawal severity may contribute to the development of AUDs.

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“…Several drugs of abuse, including alcohol (Carboni et al, 2000) and cocaine (Epping-Jordan et al, 1998), increase extracellular dopamine levels in the BNST. In addition, intracerebral self-stimulation (ICSS) in the BNST supports operant behavior in alcohol-preferring (P) but not nonalcohol-preferring (NP) rats (Eiler et al, 2007) and is a substrate for heightened sensitivity to the anxiogenic effects of corticotropin-releasing factor in Marchigian AlcoholPreferring (msP) rats (Ciccocioppo et al, 2003a). Additionally, elevations in BNST excitatory transmission have been linked to behavioral responses reinforced by cocaine and food, but not to either reward when given passively (Dumont et al, 2005).…”

Section: Neuroplasticity In Mglurmentioning

confidence: 99%

Enhanced Sensitivity to Attenuation of Conditioned Reinstatement by the mGluR2/3 Agonist LY379268 and Increased Functional Activity of mGluR2/3 in Rats with a History of Ethanol Dependence

Kufahl

Martin‐Fardon

Weiss

2011

Neuropsychopharmacol

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Recent findings implicate group II metabotropic glutamate receptors (mGluR 2/3 ) in the reinforcing and dependence-inducing actions of ethanol and identify these receptors as treatment targets for alcoholism. Here, we investigated the effects of mGLuR 2/3 activation on conditioned reinstatement in rats with different ethanol-dependence histories and examined dependence-associated changes in the functional activity of mGluR 2/3 . Following ethanol self-administration training and conditioning procedures, rats were made ethanol dependent, using ethanol vapor inhalation, under three conditions: a single intoxication and withdrawal episode (SW), repeated cycles of intoxication and withdrawal (RW), or no intoxication (CTRL). At 1 week after removal from ethanol vapor, self-administration resumed until stable baseline performance was reached, followed by extinction of operant responding and reinstatement tests. Post-withdrawal self-administration was increased in the RW group, but all groups showed conditioned reinstatement. The mGluR 2/3 agonist LY379268 dose -dependently reduced reinstatement in all groups, but was more effective at low doses in the SW and RW groups. The highest dose of LY379268 tested reduced spontaneous locomotor activity and operant responding maintained by a non-drug reinforcer, without differences among groups. The heightened sensitivity to the effects of LY379268 in rats with an ethanol-dependence history was therefore specific to behavior motivated by ethanol-related stimuli. Both the SW and RW groups showed elevated [35 S]GTPgS binding in the central nucleus of the amygdala (CeA) and bed nucleus of stria terminalis (BNST), relative to the CTRL group. The findings implicate changes in mGluR 2/3 functional activity as a factor in ethanol dependence and support treatment target potential of mGlu 2/3 receptors for craving and relapse prevention.

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Responding for brain stimulation reward in the bed nucleus of the stria terminalis in alcohol‐preferring rats following alcohol and amphetamine pretreatments

Cited by 12 publications

References 54 publications

Alcohol, Cocaine, and Brain Stimulation‐Reward in C57Bl6/J and DBA2/J Mice

Alcohol, Cocaine, and Brain Stimulation‐Reward in C57Bl6/J and DBA2/J Mice

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Enhanced Sensitivity to Attenuation of Conditioned Reinstatement by the mGluR2/3 Agonist LY379268 and Increased Functional Activity of mGluR2/3 in Rats with a History of Ethanol Dependence

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