25 Citazioni (Scopus)


Acetaldehyde, the first metabolite of ethanol, is active in the central nervous system, where it exerts motivational properties.Acetaldehyde is able to induce drinking behaviour in operant-conflict paradigms that resemble the core features of theaddictive phenotype: drug-intake acquisition and maintenance, drug-seeking, relapse and drug use despite negativeconsequences. Since acetaldehyde directly stimulates dopamine neuronal firing in the mesolimbic system, the aim of thisstudy was the investigation of dopamine D2-receptors’ role in the onset of the operant drinking behaviour for acetaldehydein different functional stages, by the administration of two different D2-receptor agonists, quinpirole and ropinirole. Ourresults show that acetaldehyde was able to induce and maintain a drug-taking behaviour, displaying an escalation duringtraining, and a reinstatement behaviour after 1-week forced abstinence. Acetaldehyde operant drinking behaviour involvedD2-receptor signalling: in particular, quinpirole administration at 0.03 mg/kg, induced a significant decrease in the numberof lever presses both in extinction and in relapse. Ropinirole, administered at 0.03 mg/kg during extinction, did not produceany modification but, when administered during abstinence, induced a strong decrease in acetaldehyde intake in thefollowing relapse session. Taken together, our data suggest that acetaldehyde exerts its own motivational properties,involving the dopaminergic transmission: indeed, activation of pre-synaptic D2-receptors by quinpirole, during extinctionand relapse, negatively affects operant behaviour for acetaldehyde, likely decreasing acetaldehyde-induced dopaminerelease. The activation of post-synaptic D2-receptors by ropinirole, during abstinence, decreases the motivation to theconsecutive reinstatement of acetaldehyde drinking behaviour, likely counteracting the reduction in the dopaminergic tonetypical of withdrawal. These data further strengthen the evidence that acetaldehyde may play a crucial role as mediator ofethanol’s central effects
Lingua originaleEnglish
Numero di pagine9
RivistaPLoS One
Stato di pubblicazionePublished - 2014

All Science Journal Classification (ASJC) codes

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  • ???subjectarea.asjc.1100.1100???
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