No abstract

Three naive pigeons were exposed to a series of two-component multiple schedules of response-independent food presentation. The component schedules were sometimes identical (non-differential procedures) and sometimes different (differential procedures). High rates of key pecking were nmaintained in all the differential procedures, and pecking decreased substantially in non-differential procedures, even when the frequency of food presentation in non-differential procedures was higher than in differential procedures. It is suggested that the high rates of key pecking were maintained not by adventitious response-reinforcer contingencies, but by differential contingencies between the stimulus (keylight) and food.The role of such contingencies in the phenomenon of behavioral contrast is discussed.If a pigeon that has been trained to peck on an illuminated key to produce food is then exposed to a procedure in which food delivery occurs witlhout regard to its behavior (response-independent food presentation), the response is nevertheless maintained at nonzero rates (Appel and Hiss, 1962;Edwards, West, and Jackson, 1968;Herrnstein, 1966;Herrnstein and Morse, 1957;Lachter, 1971;Neuringer, 1970;Zeiler, 1968). Similar findings have been reported with rats and bar pressing (Edwards, et al., 1968;Lattal and Mazey, 1971;Rescorla and Skucy, 1969; Skinner, 1938, pp. 163-166). This phenomenon has typically been explained as a corollary of the effects of response-dependent reinforcement (e.g., Herrnstein, 1966 again precede it. In this fashion, responseindependent food presentation can maintain a given class of behavior. However, since an explicit dependency between the behavior and the food is absent, the organism at times will obtain food with an appreciable delay since the last occurrence of the behavior in question, or immediately after engaging in any of a number of different behaviors. Thus, behavior other than the one being measured will also be strengthened, which is consistent with the observation that responding is maintained at a lower rate by response-independent than by response-dependent food presentation.However, an alternative account of the effectiveness of response-independent food presentation in maintaining key pecking in the pigeon has been offered by Staddon and Simmellhag (1971). They argued that the presence of food in a situation, combined with a pigeon's state of food deprivation, will induce the pigeon to peck in that situation. Moreover, they reported that while pigeons engaged in a wide variety of behaviors in the time intervals between response-independent food presentations, in the time just before delivery of the food, all pigeons were pecking. They further suggested that the rate of pecking is no lower when food delivery is responseindependent than when it is response-dependent: the difference in pecking between the two situations is that the locus of the peck is more variable when food delivery is response-1973, 19, 65-72 NUMBER I (JANUARY)

The pigeon's so-called "arbitrary" response of pecking an illuminated disk can be established and maintained by procedures resembling those of classical conditioning. This phenomenon was shown to be independent of the specific signaling relationships between illumination of the pecking disk and presentation of food; it will appear as long as the key is differentially associated with food. When a nondifferential condition is introduced, pecking "extinguishes" even if it has previously been established and even when the new condition involves as much reinforcement as the old one. Reinstating differential conditions reestablishes pecking. The initial conditions determine the speed and apparently the asymptote of pecking rates in the differential condition; initial exposure to a nondifferential procedure retards subsequent acquisition, possibly quite permanently. These findings are discussed in the context of mechanisms of adaptive learning, not involving reward and punishment, which lead to selection of effective behaviors on a nonarbitrary basis.

In neurological and behavioral studies in mice, rats, dogs and squirrel monkeys, the imidazobenzodiazepinone Ro 15-1788 acted as a potent benzodiazepine antagonist. The antagonistic activity was both preventive and curative and seen at doses at which no intrinsic effects were detected. It was highly selective in that it acted against CNS effects induced by benzodiazepines but not against those produced by other depressants, such as phenobarbitone, meprobamate, ethanol, and valproate. The onset of action was rapid even after oral administration. Depending on the animal species studied, the antagonistic effects lasted from a few hours to 1 day. The acute and subacute toxicity of Ro 15-1788 was found to be very low. Benzodiazepine-like effects were not seen.

The effect of aniracetam (Ro 13-5057, 1-anisoyl-2-pyrrolidinone) was studied on various forms of experimentally impaired cognitive functions (learning and memory) in rodents and produced the following effects: (1) almost complete prevention of the incapacity to learn a discrete escape response in rats exposed to sublethal hypercapnia immediately before the acquisition session; (2) partial (rats) or complete (mice) prevention of the scopolamine-induced short-term amnesia for a passive avoidance task; (3) complete protection against amnesia for a passive avoidance task in rats submitted to electroconvulsive shock immediately after avoidance acquisition; (4) prevention of the long-term retention- or retrieval-deficit for a passive avoidance task induced in rats and mice by chloramphenicol or cycloheximide administered immediately after acquisition; (5) reversal, when administered as late as 1 h before the retention test, of the deficit in retention or retrieval of a passive avoidance task induced by cycloheximide injected 2 days previously; (6) prevention of the deficit in the retrieval of an active avoidance task induced in mice by subconvulsant electroshock or hypercapnia applied immediately before retrieval testing (24 h after acquisition). These improvements or normalizations of impaired cognitive functions were seen at oral aniracetam doses of 10-100 mg/kg. Generally, the dose-response curves were bell-shaped. The mechanisms underlying the activity of aniracetam and its 'therapeutic window' are unknown. Piracetam, another pyrrolidinone derivative was used for comparison. It was active only in six of nine tests and had about one-tenth the potency of aniracetam. The results indicate that aniracetam improves cognitive functions which are impaired by different procedure and in different phases of the learning and memory process.