Greater ethanol inhibition of presynaptic dopamine release in C57BL/6J than DBA/2J mice: Role of nicotinic acetylcholine receptors

Yorgason, Jordan T.; Rose, Jamie H.; McIntosh, J. Michael; Ferris, Mark J.

doi:10.1016/j.neuroscience.2014.10.052

Cited by 21 publications

(29 citation statements)

References 69 publications

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“…Similarly, an in vivo FSCV study in awake, behaving rats showed that alcohol administration resulted in an increase in phasic dopamine release (Shnitko and Robinson 2015). In contrast, ex vivo FSCV studies show that acute application of alcohol to brain slices results in a reduction of phasic dopamine release in the NAc of both rodents and monkeys (Siciliano et al 2016b; Yorgason et al 2014, 2015), which is dependent on alcohol concentration and frequency of stimulation. Reductions in dopamine release in these experiments were observed only at high concentrations of alcohol (80 mM and above) and during high frequency of stimulation (20 Hz and above) (Yorgason et al 2015).…”

Section: Dopamine Signaling Following Chronic Alcohol Exposurementioning

confidence: 88%

“…In contrast, ex vivo FSCV studies show that acute application of alcohol to brain slices results in a reduction of phasic dopamine release in the NAc of both rodents and monkeys (Siciliano et al 2016b; Yorgason et al 2014, 2015), which is dependent on alcohol concentration and frequency of stimulation. Reductions in dopamine release in these experiments were observed only at high concentrations of alcohol (80 mM and above) and during high frequency of stimulation (20 Hz and above) (Yorgason et al 2015). While these findings may seem in opposition, the inconsistencies between in vivo (enhanced release) and ex vivo (reduced release) are likely driven by the fact that dopamine terminals are separated from the cell body in ex vivo slice preparations.…”

Section: Dopamine Signaling Following Chronic Alcohol Exposurementioning

confidence: 88%

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Cross-Species Alterations in Synaptic Dopamine Regulation After Chronic Alcohol Exposure

Siciliano

Karkhanis

Holleran

et al. 2018

Handbook of Experimental Pharmacology

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Alcohol use disorders are a leading public health concern, engendering enormous costs in terms of both economic loss and human suffering. These disorders are characterized by compulsive and excessive alcohol use, as well as negative affect and alcohol craving during abstinence. Extensive research has implicated the dopamine system in both the acute pharmacological effects of alcohol and the symptomology of alcohol use disorders that develop after extended alcohol use. Preclinical research has shed light on many mechanisms by which chronic alcohol exposure dysregulates the dopamine system. However, many of the findings are inconsistent across experimental parameters such as alcohol exposure length, route of administration, and model organism. We propose that the dopaminergic alterations driving the core symptomology of alcohol use disorders are likely to be relatively stable across experimental settings. Recent work has been aimed at using multiple model organisms (mouse, rat, monkey) across various alcohol exposure procedures to search for commonalities. Here, we review recent advances in our understanding of the effects of chronic alcohol use on the dopamine system by highlighting findings that are consistent across experimental setting and species.

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Section: Dopamine Signaling Following Chronic Alcohol Exposurementioning

confidence: 88%

Section: Dopamine Signaling Following Chronic Alcohol Exposurementioning

confidence: 88%

Cross-Species Alterations in Synaptic Dopamine Regulation After Chronic Alcohol Exposure

Siciliano

Karkhanis

Holleran

et al. 2018

Handbook of Experimental Pharmacology

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“…OCT3 expression has also been observed on DAT+ neurons (Mayer et al., 2018), suggesting possible co‐expression at dopamine terminals. Interestingly, OCT3 also appears to be present on striatal cholinergic neurons (Vialou, Balasse, Dumas, Giros, & Gautron, 2007), which strongly regulate terminal dynamics in the nucleus accumbens (Melchior, Ferris, Stuber, Riddle, & Jones, 2015; Siciliano, McIntosh, Jones, & Ferris, 2017; Yorgason, Rose, McIntosh, Ferris, & Jones, 2015). Therefore, it is possible that there may be additional effects of OCT3 activity on cholinergic neurons, which may alter catecholamine clearance kinetics.…”

Section: Discussionmentioning

confidence: 99%

Organic cation transporter 3 and the dopamine transporter differentially regulate catecholamine uptake in the basolateral amygdala and nucleus accumbens

Holleran

Rose

Fordahl

et al. 2020

Eur J of Neuroscience

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Regional alterations in kinetics of catecholamine uptake are due in part to variations in clearance mechanisms. The rate of clearance is a critical determinant of the strength of catecholamine signaling. Catecholamine transmission in the nucleus accumbens core (NAcc) and basolateral amygdala (BLA) is of particular interest due to involvement of these regions in cognition and motivation. Previous work has shown that catecholamine clearance in the NAcc is largely mediated by the dopamine transporter (DAT), but clearance in the BLA is less DAT-dependent. A growing body of literature suggests that organic cation transporter 3 (OCT3) also contributes to catecholamine clearance in both regions. Consistent with different clearance mechanisms between regions, catecholamine clearance is more rapid in the NAcc than in the BLA, though mechanisms underlying this have not been resolved. We compared the expression of DAT and OCT3 and their contributions to catecholamine clearance in the NAcc and BLA. We found DAT protein levels were ~ 4-fold higher in the NAcc than in the BLA, while OCT3 protein expression was similar between the two regions. Immunofluorescent labeling of the two transporters in brain sections confirmed these findings. Ex vivo voltammetry demonstrated that the magnitude of catecholamine release was greater, and the clearance rate was faster in the NAcc than in the BLA. Additionally, catecholamine clearance in the BLA was more sensitive to the OCT3 inhibitor corticosterone, while clearance in the NAcc was more cocaine sensitive. These distinctions in catecholamine clearance may underlie differential effects of catecholamines on behavioral outputs mediated by these regions.

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“…However, under specific stressful conditions (e.g., forced swim), B6 exhibit higher passive responses, increased mesocortical dopamine metabolism and inhibition of NAC dopamine release and metabolism (Ventura et al, 2002) relative to D2. In contrast, D2 may be less sensitive to the inhibitory effects of alcohol on dopamine release (Brodie and Appel, 2000; Kapasova and Szumlinski, 2008; Yorgason et al, 2015) relative to B6.…”

Section: Discussionmentioning

confidence: 99%

Comparison and Functional Genetic Analysis of Striatal Protein Expression Among Diverse Inbred Mouse Strains

Parks

Giorgianni

Jones

et al. 2019

Front. Mol. Neurosci.

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C57BL/6J (B6) and DBA/2J (D2) inbred mouse strains are highly variable genetically and differ in a large number of behavioral traits related to striatal function, including depression, anxiety, stress response, and response to drugs of abuse. The genetic basis of these phenotypic differences are, however, unknown. Here, we present a comparison of the striatal proteome between B6 and D2 and relate differences at the protein level to strain differences at the mRNA level. We also leverage a recombinant inbred BXD population derived from B6 and D2 strains to investigate the role of genetic variation on the regulation of mRNA and protein levels. Finally, we test the hypothesis that differential protein expression contributes to differential behavioral responses between the B6 and D2 strain. We detected the expression of over 2,500 proteins in membrane-enriched protein fractions from B6 and D2 striatum. Of these, 160 proteins demonstrated significant differential expression between B6 and D2 strains at a 10% false discovery level, including COMT, GABRA2, and cannabinoid receptor 1 (CNR1)—key proteins involved in synaptic transmission and behavioral response. Similar to previous reports, there was little overlap between protein and transcript levels (25%). However, the overlap was greater (51%) for proteins demonstrating genetic regulation of cognate gene expression. We also found that striatal proteins with significantly higher or lower relative expression in B6 and D2 were enriched for dopaminergic and glutamatergic synapses and processes involved in synaptic plasticity [e.g., long-term potentiation (LTP) and long-term depression (LTD)]. Finally, we validated higher expression of CNR1 in B6 striatum and demonstrated greater sensitivity of this strain to the locomotor inhibiting effects of the CNR1 agonist, Δ9-tetrahydrocannabinol (THC). Our study is the first comparison of differences in striatal proteins between the B6 and D2 strains and suggests that alterations in the striatal proteome may underlie strain differences in related behaviors, such as drug response. Furthermore, we propose that genetic variants that impact transcript levels are more likely to also exhibit differential expression at the protein level.

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Greater ethanol inhibition of presynaptic dopamine release in C57BL/6J than DBA/2J mice: Role of nicotinic acetylcholine receptors

Cited by 21 publications

References 69 publications

Cross-Species Alterations in Synaptic Dopamine Regulation After Chronic Alcohol Exposure

Cross-Species Alterations in Synaptic Dopamine Regulation After Chronic Alcohol Exposure

Organic cation transporter 3 and the dopamine transporter differentially regulate catecholamine uptake in the basolateral amygdala and nucleus accumbens

Comparison and Functional Genetic Analysis of Striatal Protein Expression Among Diverse Inbred Mouse Strains

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