The effect of deprivation and satiation on secondary reinforcement developed by two methods.
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The primate orbitofrontal cortex contains the secondary taste cortex, in which the reward value of taste is represented. It also contains the secondary and tertiary olfactory cortical areas, in which information about the identity and also about the reward value of odors is represented. The orbitofrontal cortex also receives information about the sight of objects and faces from the temporal lobe cortical visual areas, and neurons in it learn and reverse the visual stimulus to which they respond when the association of the visual stimulus with a primary reinforcing stimulus (such as a taste reward) is reversed. However, the orbitofrontal cortex is involved in representing negative reinforcers (punishers) too, such as aversive taste, and in rapid stimulus-reinforcement association learning for both positive and negative primary reinforcers. In complementary neuroimaging studies in humans it is being found that areas of the orbitofrontal cortex (and connected subgenual cingulate cortex) are activated by pleasant touch, by painful touch, by rewarding and aversive taste, and by odor. Damage to the orbitofrontal cortex in humans can impair the learning and reversal of stimulus- reinforcement associations, and thus the correction of behavioral responses when these are no longer appropriate because previous reinforcement contingencies change. This evidence thus shows that the orbitofrontal cortex is involved in decoding and representing some primary reinforcers such as taste and touch; in learning and reversing associations of visual and other stimuli to these primary reinforcers; and in controlling and correcting reward-related and punishment-related behavior, and thus in emotion.
Aspiration, but not neurotoxic, lesions of the amygdala impair performance on a visual discrimination learning task in which an auditory secondary reinforcer signals which of 2 stimuli will be reinforced with food. Because aspiration lesions of the amygdala interrupt projections of the rhinal cortex traveling close to the amygdala, it was hypothesized that damage to the rhinal cortex would severely impair learning in this task. Rhesus monkeys (Macaca mulatta) were trained to solve visual discrimination problems based on an auditory secondary reinforcer, were given lesions of the rhinal cortex or the perirhinal cortex alone, and were then retested. The monkeys displayed a reliable, albeit mild, deficit in postoperative performance. It is concluded that the aspiration lesions of the amygdala that produced a severe impairment did so because they interrupted connections of temporal cortical fields beyond the rhinal cortex that are also involved in learning in this task.
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Changes in the activity of the enzyme protein kinase C (PKC) have been implicated in learning and memory consolidation, and in the induction of long-term potentiation. The precise role of PKC in memory processing is still unknown. Using 1-day-old chicks trained on a single-trial passive avoidance task, we demonstrate that inhibition of PKC activity by melittin induced retention loss, in a dose-dependent manner, in the second stage of a three-stage sequence of memory processing. The effect was lateralized to the left hemisphere of the chick forebrain. This effect of melittin was prevented by high concentrations (16-320 microM) of the PKC activator, phorbol 12-myristate 13-acetate (PMA). Furthermore, concentrations of PMA in the range 1.6 to 40 microM were shown to induce long-term memory consolidation following a weakly reinforced version of the learning task, which normally does not lead to formation of long-term memory. That these actions of PMA are attributable to PKC activation is supported by the further finding that the inactive phorbol ester 4 alpha-PDD had no effect either on melittin-induced amnesia or on memory consolidation following weakly reinforced learning. Paradoxically, concentrations of 16 microM or higher of PMA inhibited memory consolidation for the normal strongly reinforced learning trial, an effect again not observed with 40 alpha-PDD. The results are consistent with the view that PKC activity may be implicated in a pre-long-term stage of memory processing.
Two pigeons were trained on a multiple VI-1; VI-4 min schedule for food reinforcement until a stable differential rate of response was established. Each component of the multiple schedule was in effect for 10 min and was separated from the other by 1 min time out. An Estes-Skinner conditioned suppression procedure was superimposed on each component of the schedule. The relative magnitude of the suppression behavior was measured during its acquisition and extinction, and at CS durations of 100, 200, and 300 sec. The initial magnitude of the suppression behavior was less severe on the VI-1 baseline than on the VI-4, and it extinguished more rapidly on the VI-1. As the relative duration of the CS was increased, the suppression behavior became less severe on both baselines, but the initial differential magnitude in the suppression remained intact.
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This article examines the relative merits of either partial or continuous (total) success therapy as a device for reversing learned helplessness and depression in humans. College students experienced (a) no treatment followed by either abbreviated (20 trials) or extended (40 trials) continuous success therapy, (b) soluble problems followed by either abbreviated or extended continuous success therapy, (c) insoluble problems followed by either abbreviated or extended continuous success therapy, or (d) insoluble problems followed be either abbreviated or extended partial success therapy. Subsequently, subjects in all eight groups received 40 escape-extinction trials in which aversive tones were not controllable. The results of this experiment indicated that both continuous and partial success schedules were effective in reversing depressed responding (helplessness) induced by prior exposure to insoluble problems. However, only the partial success therapy schedules produced persistent escape responding in extinction. Also, across therapy procedures, extended therapy generated more response persistence in escape extinction than did abbreviated therapy. Theoretical implications of these results are discussed, and a compatible new treatment program, labeled persistence training, is introduced.
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