Acetaldehyde operant self-administration in rats: focus on D2-receptor activation.

Abstract

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 paradigm and increases DA neurons’ firing. This research aims at investigating DA2-receptor role in the reinstatement of acetaldehyde operant-drinking behaviour, following induction, maintenance and abstinence 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 of deprivation 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-drop drinking pattern that reaches regular and higher values in the last training days. Quinpirole administration produces lever press reduction in ACD group when compared to basal intake(p<0.001) and to vehicle (p<0.05;p<0.001), while when treatment is suspended, rats reinstate 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.