Pharmacology Biochemistry & Behavior, Vol. 25, pp. 693-695, 1986.©AnkhoInternational Inc. Printed in the U.S.A. 0091-3057/86$3.00 + .00 BRIEF COMMUNICATION The Effects of Apomorphine on Leverpress Shock Escape Learning in Rats' BRUCE A. MATTINGLY Department of Psychology, Morehead State University, Morehead, KY40351 Received 24 March 1986 MATTINGLY, B. A. The effects of apomorphine on leverpress shock escape learning in rats. PHARMACOL BIOCHEM BEHAV 25(3)693-695, 1986.--Four groups of rats (n = l0 each) were tested on a discrete trial leverpress shock escape task 15 rain following an intraperitoneal injection of either 0 (saline), 0.5, 1.0, or 2.0 mg/kg apomorphine hydrochloride. The results indicated that all doses of apomorphine produced a severe disruption in escape performance. This disruption was temporary, however, as all apomorphine groups were responding as quickly as the saline control rats by the end of the training session. A comparison of the effects of apomorphine with the previously reported effects of scopolamine and septal lesions on shock escape learning revealed both similarities and differences. These findings suggest that a septal lesion- induced reduction of acetylcholine levels does not simply "unleash" an antagonistic dopaminergic system. Rats Shock escape learning Apomorphine Dopaminergic mechanisms Scopolamine Cholinergic mechanisms Septal lesions Acetylcholine Dopamine Acetylcholine-dopamine balance FOLLOWING septal damage there is a significant reduction in the levels of several forebrain neurotransmitters (see [3,9]). Over the past few years we have been studying the potential involvement of these secondary neurochemical changes in the behavioral effects of septal lesions in certain aversive learning tasks [4--7]. We have found, for example, that the cholinergic antagonist, scopolamine, but not methyl- scopolamine, produces a disruption in discrete trial lever- press shock escape learning very similar to that produced by septal lesions [4]. In contrast, a depletion of brain serotonin produced by para-chlorophenylalanine (PCPA) does not af- fect the performance of rats on a leverpress shock escape task [6]. Likewise, increasing brain serotonin levels via 5-hydroxytryptophan does not affect the shock escape per- formance of either normal or septally-lesioned rats [6]. Hence, these findings suggest that a lesion-induced reduc- tion in brain acetylcholine, but not serotonin, levels may be involved in the deficient shock escape performance of rats with septal lesions. Although our previous studies suggest the involvement of cholinergic mechanisms, because of the interaction among various neurotransmitters in many central "pathways," many neurotransmitters probably play some functional role in any complex response pattern of the organism. For example, in some areas of the brain (e.g., striatum), acetyl- choline and dopamine have been found to function in precise balance such that decreasing the activity of one has more or less the same effect as mcreasing the activity of the other (see [1] for review). Moreover, recent evidence has been presented supporting a cholinergic-dopaminergic interaction in various limbic structures including the septum (e.g., [8]). It is possible, therefore, that the disruption of shock escape learning produced by scopolamine and septal lesions may be the result of an imbalance between acetylcholine-dopamine mechanisms. If so, then increasing dopaminergic activity should have an effect on leverpress shock escape perform- ance in rats similar to that produced by decreasing acetyl- choline activity with scopolamine or septal lesions. The pur- pose of the present study, therefore, was to determine whether the leverpress shock escape performance of rats would be disrupted by a drug-induced facilitation of dopaminergic activity. Consequently, groups of rats were injected with either saline (control) or the central dopaminergic agonist, apomorphine (0.5, 1.0, or 2.0 mg/kg) and then tested on a discrete trial leverpress shock escape task. METHOD Subjects Forty male Wistar albino rats were experimentally naive and approximately 90 days old on the day of testing. All rats were housed individually and maintained on ad lib food and water. A 12 hour light-dark cycle was held constant through- out the experiment. 1This research was supported by a Faculty Research Grant from Morehead State University. The author is grateful to June Spencer and Carlos Matin for their assistance in behavioral testing. 693