Literature DB >> 10888067

Reverse microdialysis of a dopamine uptake inhibitor in the nucleus accumbens of alcohol-preferring rats: effects on dialysate dopamine levels and ethanol intake.

E A Engleman1, W J McBride, A A Wilber, S R Shaikh, R D Eha, L Lumeng, T K Li, J M Murphy.   

Abstract

BACKGROUND: The mesolimbic dopamine (DA) system has been implicated in mediating the reinforcing actions of ethanol (EtOH). This study examines the effects of local perfusion of the DA uptake inhibitor GBR12909 (GBR) on (1) DA levels in the nucleus accumbens (NAc) and (2) EtOH drinking in alcohol-preferring rats.
METHODS: Stable drinking of a 15% (v/v) EtOH solution (minimum of 0.75 g/kg body weight) was established in daily 1 hr limited access sessions. Rats were then implanted with bilateral guide cannulae aimed 4 mm above the NAc. After recovery from surgery, concentric microdialysis probes (2 mm dialysis membrane surface) were inserted into the NAc. Most placements were in the shell or overlapping both shell and core. Two days later, the probes were perfused at 1.0 microl/min with artificial cerebral spinal fluid (aCSF) for at least a 90 min washout period followed by collection of five basal samples over 150 min. Rats were then perfused with either aCSF alone or 10, 25, 100, or 200 microM of GBR for 240 min on the first day of microdialysis. During the last 60 min of the drug treatment phase, rats were given their scheduled access to 15% EtOH. All rats were then perfused with aCSF for the last 90 min of the experiment. The following day, the procedure was repeated, but animals that received aCSF on the first day were given a dose of GBR and rats given GBR on the first day received only aCSF.
RESULTS: GBR perfusion increased extracellular NAc DA levels dose dependently to more than 800% of basal levels at 100 to 200 microM but failed to alter EtOH intake (p > 0.05, paired t test) at any concentration tested. Moreover, after 100 microM of GBR perfusion had terminated, the extracellular levels of DA in the NAc remained elevated for approximately 24 hr (790% of day 1 basal; p < 0.05). The increase in dialysate DA levels observed during GBR perfusion with 100 microM was significantly greater for EtOH-experienced rats than for EtOH-naïve rats [F(7,59) = 14.85, p < 0.0001, analysis of variance, Student-Newman-Keuls post hoc test].
CONCLUSIONS: The results suggest (1) that EtOH drinking experience induces neuroadaptations that increase DA release in the NAc, and (2) that additional elevation in synaptic levels of DA in the NAc does not influence the maintenance of ongoing alcohol drinking under scheduled access conditions in alcohol-preferring animals.

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Year:  2000        PMID: 10888067

Source DB:  PubMed          Journal:  Alcohol Clin Exp Res        ISSN: 0145-6008            Impact factor:   3.455


  17 in total

1.  Reinforcing properties and neurochemical response of ethanol within the posterior ventral tegmental area are enhanced in adulthood by periadolescent ethanol consumption.

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Review 2.  A Genetic Animal Model of Alcoholism for Screening Medications to Treat Addiction.

Authors:  R L Bell; S Hauser; Z A Rodd; T Liang; Y Sari; J McClintick; S Rahman; E A Engleman
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3.  Rodent ultrasonic vocalizations as biomarkers of future alcohol use: A predictive analytic approach.

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4.  Peri-adolescent alcohol consumption increases sensitivity and dopaminergic response to nicotine during adulthood in female alcohol-preferring (P) rats: Alterations to α7 nicotinic acetylcholine receptor expression.

Authors:  Robert A Waeiss; Christopher P Knight; Gustavo B Carvajal; Richard L Bell; Eric A Engleman; William J McBride; Sheketha R Hauser; Zachary A Rodd
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5.  Limited access to ethanol increases the number of spontaneously active dopamine neurons in the posterior ventral tegmental area of nondependent P rats.

Authors:  Sandra L Morzorati; Rita L Marunde; David Downey
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Review 6.  Ethanol action on dopaminergic neurons in the ventral tegmental area: interaction with intrinsic ion channels and neurotransmitter inputs.

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Review 7.  Alcohol during adolescence selectively alters immediate and long-term behavior and neurochemistry.

Authors:  Antoniette M Maldonado-Devincci; Kimberly A Badanich; Cheryl L Kirstein
Journal:  Alcohol       Date:  2010-02       Impact factor: 2.405

8.  Ethanol drinking reduces extracellular dopamine levels in the posterior ventral tegmental area of nondependent alcohol-preferring rats.

Authors:  Eric A Engleman; Elizabeth J Keen; Sydney S Tilford; Richard J Thielen; Sandra L Morzorati
Journal:  Alcohol       Date:  2011-09       Impact factor: 2.405

9.  A single, moderate ethanol exposure alters extracellular dopamine levels and dopamine d receptor function in the nucleus accumbens of wistar rats.

Authors:  Kelle M Franklin; Eric A Engleman; Cynthia M Ingraham; Joseph A McClaren; Carrie M Keith; William J McBride; James M Murphy
Journal:  Alcohol Clin Exp Res       Date:  2009-07-01       Impact factor: 3.455

10.  Ethanol potentiates dopamine uptake and increases cell surface distribution of dopamine transporters expressed in SK-N-SH and HEK-293 cells.

Authors:  D Nicole Riherd; David G Galindo; Lucretia R Krause; R Dayne Mayfield
Journal:  Alcohol       Date:  2008-06-24       Impact factor: 2.405

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