The role of dopamine in reinforcement: changes in reinforcement sensitivity induced by D1-type, D2-type, and nonselective dopamine receptor agonists

Dose-dependent changes in sensitivity to reinforcement were found when rats were treated with low, moderate, and high doses of the partial dopamine D1-type receptor agonist SKF38393 and with the nonselective dopamine agonist apomorphine, but did not change when rats were treated with similar doses of the selective dopamine D2-type receptor agonist quinpirole. Estimates of bias did not differ significantly across exposure to SKF38393 or quinpirole, but did change significantly at the high dose of apomorphine. Estimates of goodness of fit (r2) did not change significantly during quinpirole exposure. Poor goodness of fit was obtained for the high doses of SKF38393 and apomorphine. Decrements in absolute rates of responding were observed at the high dose of quinpirole and at the moderate and high doses of SKF38393 and apomorphine. Changes in r2 and absolute responding may be due to increases in stereotyped behavior during SKF38393 and apomorphine exposure that, in contrast to quinpirole, were distant from the response lever. The present data provide evidence that sensitivity to reward is affected more strongly by dopamine D1-like receptors rather than D2-like receptors, consistent with evidence from other studies investigating consummatory dopamine behavior and the tonic/phasic dopamine hypothesis.     

Involvement of the σ Receptor inPassive-Avoidance Learning in the Day-Old Chick during the Second Wave of Neuronal Activity

The specific σ-receptor agonist (+)-SKF 10047 and antagonist BD 1047 were used to investigate whether this receptor was involved in passive-avoidance training in the day-old chick. We found 300 μM (+)-SKF 10047 to be amnesic when injected into the lobus parolfactorius 5 h after training (p < .01). Higher or lower concentrations of (+)-SKF 10047 did not disrupt memory formation. The amnesia produced by the efficacious dose of (+)-SKF 10047 was reversed by the specific antagonist, BD 1047. It is suggested that the σ-receptor may exert its effect on passive-avoidance memory consolidation during the later stages of long-term memory formation by modulation of memory-related neurotransmission.     

In vitro reinforcement of hippocampal bursting: a search for Skinner's atoms of behavior.

A novel "in vitro reinforcement" paradigm was used to investigate Skinner's (1953) hypotheses (a) that operant behavior is made up of infinitesimal "response elements" or "behavioral atoms" and (b) that these very small units, and not whole responses, are the functional units of reinforcement. Our tests are based on the assumption that behavioral atoms may plausibly be represented at the neural level by individual cellular responses. As a first approach, we attempted to reinforce the bursting responses of hippocampal units in a highly reduced brain-slice preparation with local micropressure applications of behaviorally reinforcing dopaminergic drugs. The same injections were administered independently of bursting to provide a "noncontingent" control for nonspecific stimulation or facilitation of firing. It was found that the bursting responses of individual CA1 pyramidal neurons may be progressively facilitated in a dose-related manner by response-contingent (but not noncontingent) injections of dopamine itself, the dopamine D1-preferring agonist SKF 82958, the D3-preferring agonist quinpirole, and the D2-like selective agonist (+)-4-propyl-9 hydroxynapthoxazine. These findings support the conclusion that unit bursting responses can be reinforced in vitro in hippocampal slices, and they further suggest that the same dopamine receptor subtypes are involved in both cellular and behavioral operant conditioning. The results thus provide indirect support for Skinner's atoms-of-behavior hypothesis.     

Influence of intracerebroventricular administration of dopaminergic drugs on morphine state-dependent memory in the step-down passive avoidance test

The effects of dopaminergic drugs on morphine state-dependent memory of passive avoidance task were examined in mice. Pre-training administration of morphine (5mg/kg) led to state-dependent learning with impaired memory retrieval on the test day which was reversed by pre-test administration of the same dose of the opiate. The pre-test intracerebroventricular (i.c.v.) administration of the dopamine D1 receptor agonist (SKF38393), dopamine D2 receptor agonist (quinpirole) and dopamine D2 receptor antagonist (sulpiride) not only reversed the effect of pre-training morphine treatment, but also increased this action of the drug. Furthermore, the pre-test i.c.v. administration of dopamine D1 receptor antagonist (SCH23390) prevented the restoration of memory by morphine. In conclusion, the morphine-induced recovery of memory, on the test day, seems to be induced, at least in part, through dopamine receptors.