Effects of chronic alcohol exposure on dopamine uptake in rat nucleus accumbens and caudate putamen

Budygin, Evgeny A.; Oleson, Erik B.; Mathews, Tiffany A.; Läck, Anna K.; Diaz, Marvin R.; McCool, Brian A.; Jones, Sara R.

doi:10.1007/s00213-007-0812-1

Cited by 77 publications

(79 citation statements)

References 56 publications

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“…This finding appears to contrast to a recent study that demonstrated an increase in dopamine clearance in the caudate putamen (Budygin et al, 2007). One potential explanation is that the increase in striatal dopamine clearance reported by Budygin et al could be mediated through a posttranslational mechanism involving alterations in DAT function and/or subcellular localization.…”

Section: Dorsal Striatumcontrasting

confidence: 91%

“…We did not note any changes in TH expression or levels of dopamine or dopamine metabolites in the nucleus accumbens at any time point. Given the lack of temporal and spatial resolution of the neurochemical analysis we performed it is difficult to draw conclusions, but it is worth noting that this is consistent with results obtained from other groups showing no change in dopamine release properties (Budygin et al, 2007).…”

Section: Nucleus Accumbenssupporting

confidence: 83%

“…Specifically, several recent studies (Carroll et al, 2006;Budygin et al, 2007) demonstrated that chronic ethanol exposure or consumption increased dopamine uptake in the nucleus accumbens in rats. Similar findings have also been demonstrated in non-human primates (Budygin et al, 2003), suggesting that neuroadaptations in dopaminergic systems generalize across species and thus are of particular interest.…”

Section: Nucleus Accumbensmentioning

confidence: 99%

“…Chronic ethanol exposure has been reported to alter dopaminergic function via modulation of the activity of VTA dopaminergic cells (Brodie, 2002;Shen, 2003;Hopf et al, 2007). In addition to somatic effects on dopaminergic neurons, a number of studies have suggested that chronic ethanol administration can alter dopaminergic function at the level of the dopamine synapse (Casu et al, 2002;Budygin et al, 2003;Budygin et al, 2007). In particular, several studies have provided evidence for enhanced dopamine uptake in the nucleus accumbens (Carroll et al, 2006;Budygin et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Chronic ethanol exposure leads to divergent control of dopaminergic synapses in distinct target regions

Healey

Winder

Kash

2008

Alcohol

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Neuroadaptations following chronic exposure to alcohol are hypothesized to play important roles in alcohol-induced alterations in behavior, in particular increased alcohol drinking and anxiety like behavior. Dopaminergic signaling plays a key role in reward-related behavior, with evidence suggesting it undergoes modification following exposure to drugs of abuse. A large literature indicates an involvement of dopaminergic signaling in response to alcohol. Using a chronic inhalation model of ethanol exposure in mice, we have begun to investigate the effects of alcohol intake on dopaminergic signaling by examining protein levels of tyrosine hydroxylase (TH) and the dopamine transporter (DAT), as well as monoamine metabolites in three different target fields of three different dopaminergic nuclei. We have focused on the dorsal lateral bed nucleus of the stria terminalis (dBNST) because of the reported involvement of dBNST dopamine in ethanol intake, and the nucleus accumbens (NAc) and dorsal striatum because of their dense dopaminergic innervation. After either a chronic intermittent exposure (CIE) or continuous exposure (CCE) regimen, mice were killed, and tissue punches collected from the dBNST, NAc and striatum for Western analysis. Strikingly, we found divergent regulation of TH and DAT protein levels across these three regions that was dependent upon the means of exposure. These data thus suggest that distinct populations of catecholamine neurons may be differentially regulated by ethanol, and that ethanol and withdrawal interact to produce differential adaptations in these systems.

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Section: Dorsal Striatumcontrasting

confidence: 91%

Section: Nucleus Accumbenssupporting

confidence: 83%

Section: Nucleus Accumbensmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chronic ethanol exposure leads to divergent control of dopaminergic synapses in distinct target regions

Healey

Winder

Kash

2008

Alcohol

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“…Risky decisions are those where a large but uncertain reward is favored over a smaller certain reward, a process thought to be mediated by the ventral striatum (6,7). Like virtually all drugs of abuse, alcohol alters dopamine transmission within the ventral striatum, which is a primary target of midbrain dopamine neurons (8,9). Phasic increases in dopamine transmission are evoked by rewarding outcomes and associated cues (10,11), both of which have been shown to scale with the magnitude and the probability of reward (12,13).…”

mentioning

confidence: 99%

Risk preference following adolescent alcohol use is associated with corrupted encoding of costs but not rewards by mesolimbic dopamine

Nasrallah¹,

Clark

Collins³

et al. 2011

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

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Several emerging theories of addiction have described how abused substances exploit vulnerabilities in decision-making processes. These vulnerabilities have been proposed to result from pharmacologically corrupted neural mechanisms of normal brain valuation systems. High alcohol intake in rats during adolescence has been shown to increase risk preference, leading to suboptimal performance on a decision-making task when tested in adulthood. Understanding how alcohol use corrupts decision making in this way has significant clinical implications. However, the underlying mechanism by which alcohol use increases risk preference remains unclear. To address this central issue, we assessed dopamine neurotransmission with fast-scan cyclic voltammetry during reward valuation and risk-based decision making in rats with and without a history of adolescent alcohol intake. We specifically targeted the mesolimbic dopamine system, the site of action for virtually all abused substances. This system, which continuously develops during the adolescent period, is central to both reward processing and risk-based decision making. We report that a history of adolescent alcohol use alters dopamine signaling to risk but not to reward. Thus, a corruption of cost encoding suggests that adolescent alcohol use leads to long-term changes in decision making by altering the valuation of risk.

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Roux‐en‐Y gastric bypass surgery normalizes dopamine D1, D2, and DAT levels

Hamilton

Swenson²,

Hajnal

et al. 2018

Synapse

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Roux-en-Y gastric bypass surgery (RYGB) is one of the most effective treatments for morbid obesity. However, increased substance abuse following RYGB has been observed clinically. This study examined the effects of RYGB on the dopamine system to elucidate these observed changes in reward-related behavior. Rats were assigned to four groups: normal diet with sham surgery, ad libitum high fat (HF) diet with sham surgery, restricted HF diet with sham surgery, and HF diet with RYGB surgery. Following surgeries, rats were kept on their respective diets for 9 weeks before they were sacrificed. [ H]SCH 23390, [ H]Spiperone, and [ H]WIN35 428 autoradiography was performed to quantify the effects of diet and RYGB surgery on dopamine type 1-like receptor (D1R)-like, dopamine type 2-like receptor (D2R)-like, and dopamine transporter (DAT) binding. Rats on a chronic HF diet became obese with reduced D1R-like binding within the ventrolateral striatum and the nucleus accumbens core, reduced D2R-like binding in all areas of the striatum and nucleus accumbens core and shell, and reduced DAT binding in the dorsomedial striatum. Restricted HF diet rats showed similar reductions in D1R-like and D2-R-like binding as the obese rats, and reduced DAT binding within all areas of the striatum. Both RYGB and restricted HF diet rats showed similar weight reductions, with RYGB rats showing no difference in binding compared to controls. The observed changes in binding between non-treated obese rats and RYGB rats demonstrates that HF dietary effects on the dopamine system were reversed by RYGB.

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Effects of chronic alcohol exposure on dopamine uptake in rat nucleus accumbens and caudate putamen

Abstract: The DA uptake changes after chronic alcohol exposure documented here using FSCV may be associated with a compensatory response of the DA system aimed at decreasing DA signaling. Alterations in autoreceptor function may require relatively long lasting alcohol exposure.

Cited by 77 publications

References 56 publications

Chronic ethanol exposure leads to divergent control of dopaminergic synapses in distinct target regions

Chronic ethanol exposure leads to divergent control of dopaminergic synapses in distinct target regions

Risk preference following adolescent alcohol use is associated with corrupted encoding of costs but not rewards by mesolimbic dopamine

Roux‐en‐Y gastric bypass surgery normalizes dopamine D1, D2, and DAT levels

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