Extinction and dopamine receptor blockade after intermittent reinforcement training: Failure to observe functional equivalence

Abstract

Response decrements in an operant task produced by either extinction or by the dopamine receptor blocker pimozide were examined in three experiments which employed intermittent reinforcement schedules. In contrast to the congruency between these treatments previously observed following continuous reinforcement training, treatment with pimozide was markedly more effective than extinction in decreasing performance after training with variable interval, fixed interval, and fixed ratio reinforcement. The two treatments also produced substantially different patterns of responding. A shift from extinction to pimozide did not alter the progressive decline in response rate over days, but a shift from pimozide to extinction caused a pronounced increase of performance. These results indicate that the pimozide and extinction treatment did not produce functionally equivalent effects, and that the role of dopamine on reward processes should not be inferred from comparisons between pimozide and extinction.

Tests of functional equivalence between pimozide pretreatment, extinction and free feeding

“…However, in agreement with earlier studies (Salamone 1986;Beninger et al 1987), the pattern of withinsession response decrement following pimozide pretreatment was considerably less steep than that seen in extinction. The present results also confirm that the inter-session response decrements observed during repeated testing under pimozide are not maintained if the animals are subsequently tested drug free under extinction conditions (Mason et al 1980;Tombaugh et al 1980;Beninger 1982). Other studies (Evenden and Robbins 1983;Gramling et al 1984Gramling et al , 1987 have also found that when within-and between-session patterns of responding are examined in detail, the effects of neuroleptie pretreatment differ significantly from those of reward omission.…”

“…However, evidence from a number of sources suggests that neuroleptics do not impair stimulus evaluation (Fibiger et al 1975;Beninger 1983;Martin-Iverson et al 1987;Salamone 1987). In particular, it is clear that transfer effects between neuroleptic treatment and non-reward are asymmetric: while response decrements produced by extinction are maintained on transfer to rewarded responding under neuroleptic treatment, response decrements produced by neuroleptic treatment were not maintained on transfer to drug-free extinction (Beninger 1982;Mason et al 1980;Tombaugh et al 1980). The reduction of reinforcer efficacy by neuroleptics has therefore been assumed to result from an impairment of incentive motivation rather than from a change in evaluation of the reward (Beninger 1983;Salamone 1987).…”

Systemic blockade of D2-like dopamine receptors facilitates extinction of conditioned fear in mice

“…Early work, using the D2 antagonist, pimozide, indicated that it accelerates extinction of rewarded bar pressing in rats (Ettenberg et al 1979). However, it also causes decreases in unrewarded and rewarded behaviors independently of CS presentations (Tombaugh et al 1980). The mechanisms of these effects remain unclear.…”

The effects of haloperidol on the partial reinforcement extinction effect (PREE): implications for neuroleptic drug action on reinforcement and nonreinforcement

“…The two central explanations are motor impairment (blockade of response initiation and/or maintenance) and a reduction of the rewarding value of primary reinforcers (e.g., FiNger et al 1975;Fibiger 1978;Wise et al 1978;Anisman et al 1979;Franklin and McCoy 1979;Tombaugh et al 1979Tombaugh et al , 1980Beninger et al 1980aBeninger et al , b, 1987Ettenberg et al 1981 ;Phillips et al 1981 ;Anisman and Zacharko 1982;Beninger and Freedman 1982;Liebman 1982;Spyraki et al 1982;Wise 1982;Corradini et al 1984;Wise and Colic 1984). Recently, Ettenberg and Camp (1986a, b) have obtained impressive evidence supporting the "anhedonia" hypothesis.…”