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Administration of antimuscarinic drugs induces amnesia of aversively motivated behaviors. However, when relatively high intensities of footshock are used during training (over-reinforcement), animals become protected against such amnesic state. Moreover, the protective effect is established in a none-or-all fashion, i.e., within a series of increasing intensities a minute augmentation of footshock intensity is sufficient to reach the protective threshold. In the present experiment it was found that very low intensities of aversive stimulation (under-reinforcement), sufficient to produce learning, also protected animals from scopolamine-induced amnesia. These results suggest that acetylcholine is critically involved in memory consolidation of passive avoidance, but only within a limited range of training intensities.

The prediction was made that by increasing the synthesis of striatal acetylcholine, through local injection of its precursor choline, the acquisition of a lever-pressing response in two different autoshaping situations would be accelerated. In the first experiment, choline was injected into the striatum or parietal cortex of rats immediately after dipper training; 24 h later and during 5 consecutive days the animals were submitted to an autoshaping procedure of the operant kind. In the second experiment, choline was administered to the same regions shortly after each of three classical-operant autoshaping sessions; during the next two sessions, autoshaping contingencies of the operant kind were in effect. In both experiments choline injection into the striatum induced a marked facilitation of acquisition of the conditioned responses, although cortical injection of choline produced a milder improvement only in the first experiment. These results indicate that striatal cholinergic activity is, indeed, involved in the early phases of positively reinforced learning.

Systemic administration of anticholinergic drugs produces amnesia. To determine whether this effect can be prevented by increasing the magnitude of the learning experience, independent groups of rats were trained in passive avoidance, using a 3.0-mA footshock, and then injected with scopolamine (2, 4, 6, 8 or 12 mg/kg). When retention of the task was evaluated, a dose-dependent amnesic effect was found. When footshock intensity was increased to 6.0 and 9.0 mA, injections of 8 and 12 mg/kg of scopolamine did not produce memory impairments. These findings indicate that acetylcholine plays an important role in consolidation of passive avoidance, but it does not seem to be involved in memory processes when the magnitude of the negative reinforcer is increased.

A series of experiments examined the hypothesis that mating produced analgesia in the Syrian hamster can be blocked by opiate antagonists. The first experiment established a dose response relation to painful footshock. Females were more responsive to footshock than males (p less than 0.001). The second experiment demonstrated that ten minutes of mating reduced responsiveness of both males and females to a moderate intensity of footshock. The third experiment replicated the effect of mating on the responsiveness of males to footshock, but did not demonstrate any effect of the opiate antagonist naltrexone on mating induced analgesia. The fourth experiment demonstrated that limited mating stimulation (five intromissions) has little effect on the responsiveness of sexually inexperienced males to footshock. The fifth experiment replicated the fourth experiment using sexually experienced males and obtained comparable results. Apparently mating induced analgesia in male hamsters is not blocked by opiate antagonists and which raises questions about biological activity of reported changes in endorphin activity during mating.