1 Female Wistar rats were allowed to self-administer nicotine solutions through indwelling jugular vein cannulae for 23 h per day for periods from three to five weeks. 2 Two response levers were available to the rats; responding on one lever, designated the active lever, produced an immediate infusion of nicotine solution or saline. A second lever for which responding had no programmed consequences was introduced as a control for the locomotor stimulant action of low doses of nicotine. 3 Baseline lever response rates were determined over a period of one week, in which active lever responding produced an infusion of saline. Rats were then allowed access to varying doses of nicotine or saline for a further two or three weeks. Response rates on the active lever increased significantly in rats with access to nicotine at a dose of 30 Htg kg-' per response. However, control lever response rates were also significantly elevated. 4 The role of nicotine-induced locomotor stimulation in the self-administration behaviour was further evaluated in a dose-reduction experiment, in which the dose of nicotine available to rats responding for 30 tig kg-I per response was reduced to 3 ttg kg-per response. This resulted in a significant differential increase in active lever responding relative to control lever responding. 5 The results suggest that nicotine is positively reinforcing in rats which had not previously been deprived of food or water or received prior drug treatment, but also indicate that nicotine induced locomotor stimulation may contribute to the observed increases in lever response rates when rats self-administer nicotine.

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The purpose of this study was to examine if morphine, a drug of abuse, exerts site-specific effects on intracranial self-stimulation (ICSS). Rats, implanted with dorsal brainstem (DB) and hypothalamic (HYP) electrodes, bar-pressed for ICSS at two current intensities eight hours a day during six days each of predrug saline, morphine (2.5, 5.0, 7.5 or 10.0 mg/kg) and postdrug saline conditions. There were three patterns of drug effects: "pure" depressions, "pure" facilitations and a biphasic pattern (depressions followed by facilitations). Repeated morphine administration modified the temporal patterning of these effects: shortened duration of depressions and produced earlier onsets of facilitations. Within an animal, DB electrodes displayed more depressions than the HYP electrodes. Tolerance to the depressant effects, observed frequently, occurred occasionally to the facilitative effects of morphine. The drug effects on ICSS were dissociated from those observed on other behavioral measures, and thus are not artifacts of concomitant changes in activity levels.

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