Loss of alternative non-drug reinforcement induces relapse of cocaine-seeking in rats: role of dopamine D(1) receptors - PubMed (original) (raw)
Loss of alternative non-drug reinforcement induces relapse of cocaine-seeking in rats: role of dopamine D(1) receptors
Stacey L Quick et al. Neuropsychopharmacology. 2011 Apr.
Abstract
Animal models of relapse to drug seeking have focused primarily on relapse induced by exposure to drugs, drug-associated cues or contexts, and foot-shock stress. However, relapse in human drug abusers is often precipitated by loss of alternative non-drug reinforcement. The present experiment used a novel 'resurgence' paradigm to examine relapse to cocaine seeking of rats as a result of loss of an alternative source of non-drug reinforcement. Rats were first trained to press a lever for intravenous infusions of cocaine. Next, cocaine deliveries were omitted and food pellets were provided for an alternative nose-poke response. Once cocaine seeking was reduced to low levels, food pellets for the alternative response were also omitted. Cocaine seeking increased with the loss of the alternative non-drug reinforcer (ie, resurgence occurred) despite continued extinction conditions. The increase in cocaine seeking did not occur in another group of rats injected with SCH 23390 before the loss of the alternative reinforcer. These results suggest that removal of an alternative source of reinforcement may induce relapse of cocaine seeking and that the dopamine D(1) receptor may have a role in this effect.
Figures
Figure 1
Resurgence of cocaine seeking. Lever pressing (cocaine) and nose poking (food) for the control and SCH 23390 groups across experimental phases. When an alternative source of food reinforcement was removed during the resurgence and resurgence 2 conditions, rates of extinguished lever pressing for cocaine increased for the control group, but not for the SCH 23390 group. Data are from the last five sessions of the baseline and the two extinction+food phases and from the first five and three sessions of the resurgence and resurgence 2 phases, respectively.
Figure 2
Within-session patterns of responding. Cumulative lever presses across successive 2-min bins of the first resurgence session for the control and SCH 23390 groups. Similar data for the last session of exposure to the extinction+food phase (combined across groups) are provided for comparison. Lever pressing for the control and SCH 23390 groups did not differ until the 4th 2-min bin. In addition, lever pressing for the SCH 23390 continued to occur at a low rate throughout the session, as was true for the last extinction+food session.
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