Acetaldehyde (ACD), ethanol first metabolite, is rewarding in rodents and humans; it induces“place preference”, is self-administer directly in the VTA, orally in an operant/conflict paradigmand increases DA neurons’ firing. This research aims at investigating DA2-receptor role in thereinstatement of acetaldehyde operant-drinking behaviour, following induction, maintenance andabstinence in the rat. Male Wistar rats are trained to orally self-administer ACD solution (3.2% v/v)or water, in an operant chamber under a FR1. Afterwards animals undergo cyclic periods ofdeprivation and relapse to ACD. The effect ofD2-receptor activation by quinpirole (0.03mg/kg,i.p.)on operant ACD self-administration is tested during relapse sessions. Rats show a peak-and-dropdrinking pattern that reaches regular and higher values in the last training days. Quinpiroleadministration produces lever press reduction in ACD group when compared to basalintake(p<0.001) and to vehicle (p<0.05;p<0.001), while when treatment is suspended, ratsreinstate lever presses for ACD. ACD incentive properties involve dopamine neurotransmission:D2-receptor activation is able to reduce reinstatement of operant drinking behaviour for ACD, following periods of abstinence, probably acting at a pre-synaptic level, thus reducing DA release in mesolimbic areas. These findings further support ACD pivotal role in ethanol central effects.
|Numero di pagine||515|
|Stato di pubblicazione||Published - 2013|