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Neural systems implicated in delayed and probabilistic reinforcement.

This review considers the theoretical problems facing agents that must learn and choose on the basis of reward or reinforcement that is uncertain or delayed, in implicit or procedural (stimulus-response) representational systems and in explicit or declarative (action-outcome-value) representational systems. Individual differences in sensitivity to delays and uncertainty may contribute to impulsivity and risk taking. Learning and choice with delayed and uncertain reinforcement are related but in some cases dissociable processes. The contributions to delay and uncertainty discounting of neuromodulators including serotonin, dopamine, and noradrenaline, and of specific neural structures including the nucleus accumbens core, nucleus accumbens shell, orbitofrontal cortex, basolateral amygdala, anterior cingulate cortex, medial prefrontal (prelimbic/infralimbic) cortex, insula, subthalamic nucleus, and hippocampus are examined.

Animals↗

The limits and motivating potential of sensory stimuli as reinforcers for autistic children.

This study investigated the reinforcing properties, limits, and motivating potentials of sensory stimuli with autistic children. In the first phase of the study, four intellectually retarded autistic children were exposed to three different types of sensory stimulation (vibration, music, and strobe light) as well as edible and social reinforcers for ten-second intervals contingent upon six simple bar pressing responses. In the second phase, the same events were used as reinforcers for correct responses in learning object labels. The results indicated that: (a) sensory stimuli can be used effectively as reinforcers to maintain high, durable rates of responding in a simple pressing task; (b) ranked preferences for sensory stimuli revealed a unique configuration of responding for each child; and (c) sensory stimuli have motivating potentials comparable to those of the traditional food and social reinforcers even when training receptive language tasks.

Autistic Disorder↗

The effects of interval duration on temporal tracking and alternation learning.

On cyclic-interval reinforcement schedules, animals typically show a postreinforcement pause that is a function of the immediately preceding time interval (temporal tracking). Animals, however, do not track single-alternation schedules-when two different intervals are presented in strict alternation on successive trials. In this experiment, pigeons were first trained with a cyclic schedule consisting of alternating blocks of 12 short intervals (5 s or 30 s) and 12 long intervals (180 s), followed by three different single-alternation interval schedules: (a) 30 s and 180 s, (b) 5 s and 180 s, and (c) 5 s and 30 s. Pigeons tracked both schedules with alternating blocks of 12 intervals. With the single-alternation schedules, when the short interval duration was 5 s, regardless of the duration of the longer interval, pigeons learned the alternation pattern, and their pause anticipated the upcoming interval. When the shorter interval was 30 s, even when the ratio of short to long intervals was kept at 6:1, pigeons did not initially show anticipatory pausing-a violation of the principle of timescale invariance.

Animals↗

Frequency of reinforcement as a determinant of extinction-induced aggression during errorless discrimination learning.

Seven pigeons were trained to discriminate without errors between a green keylight and a dark key. The key-pecking response was reinforced in the presence of green, and extinction was in effect in the presence of the dark key. The opportunity to attack a restrained target pigeon was present only during extinction. Both variable-interval 30-sec and fixed-ratio 1 schedules of reinforcement during the positive stimulus induced a higher rate of attack during extinction than a variable-interval 5-min schedule. The highest rate of attack during extinction occurred during the first 20 sec after the positive stimulus terminated. Hence, the withdrawal of the positive condition, rather than the consequences of the pecking response during extinction, appears to be one of the primary factors responsible for attack between pigeons during extinction. Behavioral contrast, defined as a decrease in the rate of responding when the positive stimulus was presented alone, was obtained from the four birds that displayed the lowest overall rates of attack while the three birds with the highest attack rates did not display behavioral contrast. For the birds without contrast, components of the attack response during the positive stimulus presumably competed with and reduced the rate of pecking the key, thereby recluding behavioral contrast.

Aggression↗

Primary reinforcing effects of nicotine are triggered from multiple regions both inside and outside the ventral tegmental area.

Nicotine is thought to be the key substance responsible for tobacco-smoking habits and appears to trigger reinforcement via the ventral tegmental area (VTA). Recently, multiple anatomical substrates for drug reinforcement have been identified in the vicinity of the ventral midbrain. In addition to the posterior portion of the VTA, the central linear nucleus raphé and the supramammillary nucleus of the posterior hypothalamus mediate drug reinforcement. Using intracranial self-administration procedures, we examined whether these regions mediate the reinforcing effects of nicotine. Rats learned to lever press for self-administration of nicotine into the posterior VTA, central linear nucleus, and supramammillary nucleus, suggesting a reinforcing action of nicotine in these regions. The rats did not self-administer nicotine into surrounding regions including the anterior VTA, substantia nigra, the region just dorsal to the posterior VTA, interpeduncular nucleus, or medial mammillary nucleus. The reinforcing effects of nicotine into the three brain regions were further confirmed by a two-lever discrimination procedure, in which rats learned to selectively respond between active and inactive levers. The reinforcing effects of nicotine administration into the posterior VTA, central linear nucleus, and supramammillary nucleus were blocked by coadministration of the nicotine receptor antagonist mecamylamine. The reinforcing effects of nicotine into the posterior VTA or central linear nucleus were attenuated by coadministration of the D2 receptor agonist quinpirole. These findings demonstrate that nicotine reinforcement involves multiple regions both inside and outside the VTA.

Animals↗