Elsevier

Alcohol

Volume 13, Issue 6, November–December 1996, Pages 569-574
Alcohol

Article
Serotonin-3 receptor and ethanol-stimulated somatodendritic dopamine release

https://doi.org/10.1016/S0741-8329(96)00069-9Get rights and content

Abstract

The effects of local application of the 5-HT3 receptor agonist, 1-(m-chlorophenyl)-biguanide (CPBG), and IP administration of ethanol on the extracellular levels of dopamine (DA) in the ventral tegmental area (VTA) were studied using in vivo microdialysis. Adult female Wistar rats were implanted with microdialysis probes in the VTA at least 24 h before each experiment. Stable extracellular levels of DA (101 ± 9 fmol/20 min) were established before initiating the experiments. Application of 10–250 μM CPBG through the microdialysis probe dosedependently enhanced the extracellular concentrations of DA but did not alter the levels of either 3,4-dihydroxyphenylacetic acid or homovanillic acid in the dialysate. The effects of CPBG were reversible and dependent upon Ca2+. Co-perfusion with the 5-HT3 receptor antagonist, 3-tropanyl-indole-3-carboxylate (ICS 205-930), inhibited the effects of CPBG on enhancing extracellular DA levels. The IP administration of 2g/kg ethanol significantly (p < 0.005) enhanced the levels of DA to 150% of baseline values; this ethanol-induced increase was prevented by local perfusion with 100 μM ICS 205–930. These results suggest that 5-HT3 receptors in the VTA are involved in regulating the somatodendritic release of DA and in mediating the stimulatory effects of ethanol on this neuronal system.

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    Additionally, we did not detect changes in the rate of decay of the signal in the nAcc of animals that received systemic administration of the serotonin reuptake inhibitor fluoxetine (10 mg/kg, i.p.), suggesting that serotonin was not released in a detectable fashion in the nAcc core after DR stimulation (Figure S4D). Because previous in vivo microdialysis studies have shown that 5-HT3 receptors affect dopamine release within the mesoaccumbens system (Campbell et al., 1996; Imperato and Angelucci, 1989; McBride et al., 2004), we tested the effect of ondansetron on evoked accumbal dopamine release driven by DR electrical stimulation. We found that the baseline (predrug) level of dopamine release in nAcc core evoked by DR electrical stimulation (Figures S4E–S4G; 141.9 ± 8.8 nM, n = 4) was significantly reduced by systemic application of ondansetron (2 mg/kg i.p.) (Figure S4E; 89.4 ± 5.0 nM, p < 0.01, n = 4).

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