Decreased intracranial self-stimulation after neuroleptics or 6-hydroxydopamine: evidence for mediation by motor deficits rather than by reduced reward.

Abstract

Rats were implanted with electrodes in the lateral hypothalamus, put on a 22-h food deprivation schedule and trained to bar-press for ICS and for food on a CRF schedule. Haloperidol (0.08 mg/kg) and pimozide (0.22 mg/kg) significantly decreased responding for both reinforces, although responding for ICS was decreased more than it was for food. The same doses of these drugs did not decrease food consumption of a 15-min ad libitum test after 22-h of food deprivation, suggesting that the decreased bar-pressing for food was not the result of anorexia or reduced motivation for food. When similar rates of responding for ICS and for food were obtained on a V1 60 schedule, haloperidol (0.1 mg/kg) reduced responding for food and ICS to a similar extent. Thus, when baseline rate is controlled for, neuroleptics do not selectively reduce responding for ICS. In addition, examination of cumulative response records revealed that rather than producing an extinction curve, as would be predicted if neuroleptics reduced the rewarding properties of ICS, haloperidol produced a uniform decrease in the rate of responding throughout the experimental session. Similar results were obtained with intraventricular 6-hydroxydopamine (6-OHDA) injections. While these experiments do not exclude the possibility that dopaminergic (DA) systems participate in some central reinforcement mechanisms, they suggest that neuroleptics and 6-OHDA decrease responding for food or ICS primarily by impairing the function of DA systems critically involved in the initiation or maintenance of operant behaviour rather than by interfering with reward.