Abstract
RationaleEthanol has rewarding and aversive properties, and the balance of these properties influences voluntary ethanol consumption. Preclinical and clinical evidence show that the aversive properties of ethanol limit intake. The neural circuits underlying ethanol-induced aversion learning are not fully understood. We have previously shown that the lateral habenula (LHb), a region critical for aversive conditioning, plays an important role in ethanol-directed behaviors. However, the neurocircuitry through which LHb exerts its actions is unknown.ObjectiveIn the present study, we investigate a role for the rostromedial tegmental nucleus (RMTg), a major LHb projection target, in regulating ethanol-directed behaviors.MethodsRats received either sham or RMTg lesions and were studied during voluntary ethanol consumption; operant ethanol self-administration, extinction, and yohimbine-induced reinstatement of ethanol-seeking; and ethanol-induced conditioned taste aversion (CTA).ResultsRMTg lesions increased voluntary ethanol consumption and accelerated extinction of ethanol-induced CTA.ConclusionsThe RMTg plays an important role in regulating voluntary ethanol consumption, possibly by mediating ethanol-induced aversive conditioning.
Highlights
Drugs of abuse, including ethanol, have both rewarding and aversive properties (Verendeev and Riley 2013), and the relative balance of these properties importantly influences levels of voluntary drug intake (Riley 2011)
rostromedial tegmental nucleus (RMTg) lesion had no significant effect on water intake (no significant main effect of lesion, F(1.51) = 1.8, p = 0.18, and no significant interaction of lesion and drinking session, F(5.1, 258.5) = 0.5, p = 0.8)
We compared intake in rats with low and high levels of damage; we found no significant differences in these groups with respect to ethanol intake in the intermittent ethanol access (IEA) paradigm (Table 2)
Summary
Drugs of abuse, including ethanol, have both rewarding and aversive properties (Verendeev and Riley 2013), and the relative balance of these properties importantly influences levels of voluntary drug intake (Riley 2011). For heavy drinkers, decreased levels of aversive sedation are predictive of increased ethanol-binge frequency, as well as increased likelihood of developing an alcohol-use disorder. These results show that in humans, decreased sensitivity to the aversive effects of ethanol is strongly associated with increased ethanol intake (King et al 2011; King et al 2014). P rats show attenuated ethanolinduced CTA relative to alcohol-non-preferring (NP) rats (Froehlich et al 1988) These data suggest that decreased sensitivity to aversive effects of ethanol may contribute to high ethanol intake in P rats. The measures of aversion included above are heterogeneous (and likely have distinct underlying mechanisms), suggesting that ethanol-induced
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