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The partial reinforcement extinction effect after treatment with chlordiazepoxide.

Two experiments are reported, in which rats were run in a straight alley for food reward with or without injections of the anti-anxiety drug, chlordiazepoxide (CDP). The experiments were directed to two questions. (1) Can one predict the effects of CDP from knowledge of the effects of a second anti-anxiety drug, sodium amylobarbitone (SA) (2) can the effects of CDP be predicted from the hypothesis that anti-anxiety drugs attenuate responses to conditioned frustrative stimuli? The experiments examined the effects of CDP on the partial reinforcement extinction effect (PREE) at one trial a day. CDP injected throughout acquisition and extinction reduced the PREE. This effect was probably due to the presence of the drug during acquisition. Injected during extinction only, CDP increased resistance to extinction in both continuous and partial reinforcement groups. These effects of CDP were closely similar to those previously reported for SA, thus answering question (1) in the affirmative. The effects of CDP on the PREE were also consistent with the conditioned-frustration hypothesis (question 2).

Amobarbital↗

Piracetam facilitates retrieval but does not impair extinction of bar-pressing in rats.

Rats were trained on a continuously reinforced bar-press response for water reward. Seven days later they were retested for retention, with or without pretest injection of the nootropic drug, piracetam. Drug-treated animals had significantly shorter response latencies than saline-treated animals. The results are interpreted as a facilitation of retrieval processes after forgetting. The experiment was extended under extinction conditions and it was found that after three sessions there was a tendency to facilitate extinction when response latency is used as the extinction index. The clinical interest of a drug which facilitates the retrieval aspect of the memory process without impairing extinction is discussed.

Animals↗

Performance and extinction of lever press behavior following chronic administration of desipramine to rats.

The effect of repeated administration of desipramine (DMI) on the acquisition, performance, and extinction of a lever press response for food reward was studied. Chronic administration of DMI caused a reduction in pressing under a CRF schedule both in naive and well-trained rats. Responding during extinction sessions did not differ between saline-treated rats and rats given DMI chronically. In addition, chronic administration of DMI reduced the body weight and food intake of rats on either a free-feeding or a restricted-feeding schedule. Consequently, lever pressing was also studied in a group of rats whose body weight was regulated to match the body weight of rats were administered DMI chronically. In comparison to this control group, rats administered DMI chronically responded significantly less during both reinforcement and extinction sessions. These results fail to replicate earlier reports that chronic DMI administration produces increased resistance to extinction. The results also show that assessment of food-motivated performance in rats treated chronically with DMI is difficult because of long-term changes in body weight and food intake.

Animals↗

Influence of housing conditions and state of partner on conditioning and extinction of taste aversion to lithium and chlorpromazine.

Rats were used in two experiments to investigate the influence of social variables on the acquisition of Conditioned Taste Aversion (CTA) to either lithium chloride (10 ml/kg IP of a 0.3-M solution given twice) or chlorpromazine (8 mg/kg IP given four times) and on subsequent extinction. CTA acquisition was not affected by original housing assignment (isolation or paired housing for 15-23 days prior to conditioning), by the shifted social assignment during conditioning, or by the drugged state of the paired animals' partners on drug-scheduled days. However, for both drugs, permanently isolated animals extinguished CTA more slowly than rats housed permanently in pairs. Shifts from isolation to pairing or vice versa failed to alter CTA extinction in the case of lithium, but affected it significantly in chlorpromazine-treated rats. Shifts from isolation to paired housing with an undrugged partner produced faster extinction for lithium than the corresponding group with a drugged partner. For chlorpromazine, the effect of the same shift was exactly the opposite. Overall, the results show that changes in CTA extinction can be a function of social variables.

Animals↗

Characteristics of extinction of a conditioned passive avoidance reflex in mice with different levels of anxiety.

The relationship between the extinction of a conditioned passive avoidance reflex and the initial anxiety level was studied in mice. The time spent in the open arms of an elevated cross maze was used to classify the mice into high-, intermediate-and low-anxiety individuals. Each level of anxiety was found to correspond to a defined extinction dynamic. Highly anxious mice were characterized by the absence of extinction of the conditioned passive avoidance reflex and stability of good reproduction of the memory trace on testing to as long as 15 days. In intermediately anxious individuals, a deficit in performance of the avoidance reflex appeared from day 7 of extinction. In low-anxiety mice, memory trace reproduction deteriorated from test day 11.

Animals↗

The effect of hypocapnia on extinction of conditioned fear responses.

Conditioning models have been very helpful in the understanding of the etiology and maintenance of anxiety. Such laboratory models, however, leave unexplained why in many cases of naturally occurring anxiety, as in the case of agoraphobia, the fear responses do not extinguish. Literature on experimental anxiety provocation suggests that a systemic alkalosis might play a role in the maintenance of phobic fear. It was hypothesized that a subject in a state of respiratory alkalosis would show delayed extinction to classical conditioned anxiety. In a differential classical conditioning paradigm, consisting of a habituation-, an acquisition-, and an extinction-phase, slides and electric shocks were used as conditioned stimuli (CS) and unconditioned stimuli (US) respectively. The skin conductance response was taken as (U)CR. Subjects were randomly assigned to two groups: hyperventilation or control. It was shown that the extinction was not delayed when subjects were hypocapnic during the extinction. These data support the view that a respiratory alkalosis per se is not a sufficient condition for the maintenance of neurotic fears. The data of the present study are discussed in the context of existing literature on a psychological interpretation of the maintenance of anxiety.

Adult↗

The dorsal bundle extinction effect:dependence on subtle changes in acquisition.

Destruction of the ascending noradrenergic innervation to the forebrain in rats by intracerebral injection of the selective neurotoxin 6-hydroxydopamine (4 microgram in 2 microliter injected bilaterally into the dorsal bundle in the mesencephalon) was found to cause resistance to extinction of a continuously reinforced lever press response. However, this effect occurred only if the lesion were present during acquisition training on the reinforced schedule and not if intact animals were trained and the lesion inflicted after completion of acquisition training and just prior to the extinction phase. Thus, the behavioural effect that manifests itself during extinction appears to be due to subtle changes in the acquisition learning process. This is consistent with the predictions of an attentional theory of noradrenergic function and appears to exclude most other suggested explanations of the dorsal bundle extinction effect.

Animals↗

Hippocampectomy disrupts the topography of the rat eyeblink response during acquisition and extinction of classical conditioning.

The effect of hippocampal lesions on acquisition and extinction of eyeblink conditioning in rats was examined with the procedure described by Schmajuk and Christiansen (Physiol. Behav., 48 (1990) 755-758). Male Long-Evans rats received either sham, cortical control or hippocampal lesions. Animals were trained in a delay conditioning paradigm with a 500-ms, 98-dB, white noise conditioned stimulus; a 150-ms, 5-psi air puff unconditioned stimulus; a 350-ms interstimulus interval; and a 60-s average intertrial interval. Each animal received 50 trials daily until it reached a criterion of 80% conditioned responses (CR) on a given day. After acquisition criterion was reached, extinction began the next day and continued until each animal achieved a criterion of one CR in a block of 10 consecutive trials. Although hippocampal lesions affected neither acquisition nor extinction rates, hippocampal lesioned animals showed significantly shorter CR onset latency during acquisition and extinction, and larger CR peak amplitude during acquisition. The results are discussed in terms of hippocampal modulation of cerebellar learning.

Animals↗

Des-Gly-vasopressin improves acquisition and slows extinction of autoshaped behavior.

The effects of a vasopressin analog (DGAVP) with minimal endocrinological activity, were assayed on acquisition and extinction of a discrete trial, food reinforced, autoshaped lever touch response. Magazine-trained rats, maintained at 80-85% of free-feeding body weights, were injected s.c. with saline, 5 or 10 micrograms/kg of DGAVP 1 h before each of two sessions in which they learned to touch a retractable lever, presented on a 45 s random interval (RI 45) schedule. Retracted lever contacts (nose-pokes) and unconditioned rearing activity were simultaneously monitored. After acquisition of the extended lever touch response, rats were reassigned to treatment groups, and again injected with saline, 5 or 10 micrograms/kg of DGAVP 1 h before each of two extinction sessions. DGAVP facilitated acquisition (5 micrograms/kg) and slowed extinction (5 and 10 micrograms/kg) of conditioned behavior, while having no effects on the other behaviors, thus demonstrating the specificity of the effect of a vasopressin-like compound on both tasks (enhanced acquisition and retarded extinction) used to study learning.

Animals↗

Comparing autistic and normal children along the dimensions of reinforcement maximization, stimulus sampling, and responsiveness to extinction.

The purpose of this study was to assess autistic children's ability to maximize reinforcement, sample among available stimuli, and respond to extinction. Responding to five concurrent reinforcement schedules (CRF, FR 2, FR 4, FR 7, and FR 11) was monitored and compared to groups of mental age-matched and chronological age-matched normal children. When a given child consistently selected a given schedule of reinforcement, it was then put on extinction, and both perseveration and responding to the remaining (intact) schedules of reinforcement were monitored. The results showed, first, that while normal children selected the richest schedule of reinforcement, autistics did not maximize reinforcement, typically selecting one of the thinner schedules available. Second, the autistic children sampled less, and less efficiently, than the normal children. Third, the autistic children proved to be much less responsive to extinction, perseverating longer than the normal children before switching to a new reinforcement schedule. Fourth, whenever extinction proved to be a problem in the autistics, it was quickly achieved by a simple change in the stimulus conditions. These results are discussed as possible "keystone" deficits, which may be causally related to many of the behavioral deficits of autism and which might be important target behaviors for treatment.

Adolescent↗

Hormonal modulation of extinction responses induced by sexual steroid hormones in rats.

A functional interrelation between the nervous and endocrine systems has been established. However, few studies have dealt with the effects of sexual steroids on learning and memory. The aim of this work was to determine whether sexual steroid hormones could modulate the extinction response of a passive avoidance conditioning in rats. Male Wistar rats, randomly assigned to five groups, two controls and three experimental groups, were submitted to a one-trial passive avoidance conditioning and tested for their retention 24 hr after and during 10 weeks. One control group received no treatment at all, the other received vegetable oil, and the three experimental received 20 mg of testosterone enanthate, 0.8 mg estradiol valerate, or 4 mg nandrolone decanoate, respectively. All substances were applied in a 0.3 ml volume, 24 hours before training and before testing for retention each week during 10 weeks. Results indicate that the extinction process is modulated by these hormones, since testosterone and estradiol facilitate extinction, whereas the anabolic androgen produced a resistance to the extinction process.

Anabolic Agents↗

Ipsilateral auditory extinction following frontal and basal ganglia lesions of the left hemisphere.

When tested on a dichotic digits listening task, patients with unilateral lesions of the left frontal lobe and left anterior basal ganglia exhibited ipsilateral auditory extinction. This phenomenon has been documented before, but only in patients with lesions involving the region posterior and lateral to the posterior aspect of the left lateral ventricle. As patients with lesions in the equivalent region of the right hemisphere also exhibit extinction of verbal material arriving in their left ears it has been hypothesized that these posterior lesions disrupt an interhemispheric pathway connecting the two temporal lobes. As it appears that the ipsilateral auditory pathways are suppressed under conditions of dichotic stimulation, such an interhemispheric pathway would be the means whereby left-ear verbal stimuli reached the left (speech) hemisphere. Therefore a disruption of this pathway could result in left-ear extinction for verbal material. The finding that left anterior lesions also result in left-ear extinction poses problems for this hypothesis and in particular for the suggested posterior route of the interhemispheric pathway.

Adolescent↗

An experimental investigation on the nature of extinction.

Under conditions of bilateral simultaneous presentation a right brain-damaged patient consistently extinguished visual stimuli presented for 200 msec to the left visual field. He was submitted to a series of experiments aimed at assessing the variables that influence this phenomenon. Extinction persisted unmodified when stimulus presentation was lengthened to 500 msec, when the size of the left stimulus was four-fold that of the right stimulus and for whatever position the stimuli occupied on the two halves of the display. Single stimuli were always perceived, but their localization was transposed rightward. The only condition in which extinction was partially reduced was when the instructions called for total disregard of the right stimulus. The patient also extinguished the leftmost of two stimuli presented in the left space, while he always perceived both stimuli when they were presented in the right space. However, if attention was covertly moved to a point in the right space and two stimuli were displayed to either side of it, left stimuli were neglected 70% of the time. Though a left stimulus was never perceived, it slowed the RT to the identification of a right stimulus. These data are interpreted in the frame of the directional bias theory, which attributes extinction to a shift of attention towards the side ipsilateral to the lesion, caused by the imbalance between the opponent turning processors, controlled by the right and left hemisphere. However, the striking difference in the rate of extinction when both stimuli were presented to the left or to the right field implies a stepwise decrement in the deployment of attention by the damaged processor, when it enters in the opposite space.

Attention↗

Dorsal bundle extinction effect: motivation or attention?

Male albino Wistar rats were injected bilaterally with 4 micrograms of 6-hydroxydopamine into the dorsal noradrenergic bundle to deplete forebrain noradrenaline to less than 5% of control values. Acquisition learning of a fixed interval schedule or a continuously reinforced schedule was not altered but resistance to extinction was seen after food reinforced training on either schedule but not after water reinforced training. A possible increase in food motivation was tested by the use of preloading with free food prior to a fixed interval session but both control and lesioned rats reacted similarly to this manipulation thus appearing to exclude an increase in food motivation. An attentional explanation is proposed and tested by the demonstration that resistance to extinction does not occur after a partially (variable ratio 4), as opposed to a continuously, reinforced schedule. Further evidence in favour of an attentional mechanism comes from the finding that on both a fixed interval and a continuously reinforced schedule the lesion has to be present during the acquisition phase to result in subsequent resistance to extinction. Intact animals trained on either schedule and subsequently subjected to the lesion failed to show an increased resistance to extinction.

Animals↗

Effects of early postnatal gonadal steroids on extinction of a continuously food-rewarded running response.

In the present work the existence of sex differences (Experiment 1) on the acquisition and extinction of a continuously reinforced response in a short and narrow runway (100 x 9 x 10 cm) were investigated. In addition to the investigation of the basic sex differences in Experiment 1, the effect of postpuberal gonadectomy of male and female rats and the role of the early postnatal gonadal steroids on these situations were also examined in Experiments 2 and 3, respectively. In all experiments, no sex differences were found in acquisition. However, males extinguished faster than female rats. Gonadectomy of both sexes in adulthood, although it increases their latencies in acquisition, did not affect the differences between sexes during extinction. In contrast, in Experiment 3 female androgenization and male orchidectomy on day one after birth reversed the direction of sex differences found between control rats in the extinction period. Our findings suggests that the observed sex differences in extinction may be due to an underlying sexual dimorphism in the response inhibition process.

Androgens↗

Reversal of extinction by scopolamine.

The aim of this experiment was to determine the effects of muscarinic blockade on extinction of passive avoidance conditioning. Rats were trained with a foot shock of 2.5, 3.0, or 6.0 mA and were tested for retention for 8 weeks (once weekly). Five minutes before the seventh test they were injected with 8 mg/kg scopolamine. The groups that had been trained with 2.5 and 3.0 mA showed extinction, which was reversed by the scopolamine; the overreinforced group (6.0 mA) did not show extinction and the scopolamine did not alter the conditioned response. The data support the hypothesis that extinction represents the learning of a new response sustained by a set of cholinergic neurons, different from that which mediated original passive avoidance learning.

Acetylcholine↗

Possible involvement of serotonin in extinction.

In Experiment 1, rats were trained to leverpress for continuous reinforcement with food; half were then intubated with the serotonin synthesis inhibitor parachlorophenylalanine (PCPA: 400 mg/kg) and half with water. In extinction the PCPA-treated rats responded at a higher rate. In Experiment 2, rats were trained on a random interval schedule and then assigned to two groups, treated as in Experiment 1, and tested in extinction. There was no significant difference in the resistance to extinction of the two groups. In Experiment 3, the responding of rats trained in a punished stepdown response paradigm and then given an intragastric injection of PCPA took longer to recover than the responding of water-injected controls. These observations suggest that serotonergic neurons might play a role in extinction processes.

Animals↗

Neurochemical basis of the dorsal bundle extinction effect.

Injection of 6-hydroxydopamine into the mesencephalon of the rat has been found to cause resistance to extinction on continuously reinforced schedules. The neurochemical basis of this effect was investigated by using another concentration of 6-hydroxydopamine and by another position of injection. Severe depletion of forebrain noradrenaline was found after these injections with no change in dopamine, serotonin, cholinergic or GABAergic parameters in any brain area measured. The noradrenergic nature of the effect was further shown by the reversal fo the usual behavioural effect following pretreatment with a noradrenaline uptake inhibitor (desimipramine, 25 mg/kg 30 min prior to intracerebral injection of 6-hydroxydopamine). This rules out non-specific damage caused by the 6-hydroxydopamine as the neurochemical basis of the dorsal bundle extinction effect. Failure to find resistance to extinction after either kainic acid or 5-7 dihydroxytryptamine injection seems also to exclude respectively cell body loss at the injection site or damage to serotonergic systems. It is concluded that the dorsal bundle extinction effect is noradrenergic in nature.

5,7-Dihydroxytryptamine↗