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J Feldon

Publications and source records attributed to J Feldon.

At least 181 records · Page 10Linked to original sources

Successful overshadowing and blocking in hippocampectomized rats.

Overshadowing (Experiment 1) and blocking (Experiment 2) were investigated using a conditioned suppression paradigm in rats. Neither hippocampectomy nor cortical control lesions affected the extent to which a salient stimulus overshadowed a less salient one. Nor did the lesions affect the extent to which a stimulus that was highly correlated with shock overshadow a stimulus that was less well correlated with shock. Finally, the lesions did not alter the extent to which a previously reinforced stimulus blocked conditioning to another stimulus when both were presented as a reinforced compound stimulus. It is thus possible for hippocampectomized rats to show apparently normal overshadowing and blocking, at least under some testing conditions.

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Anticonflict action of sodium valproate. Interaction with convulsant benzodiazepine (Ro 5-3663) and imidazodiazepine (Ro 15-1788).

The possibility that Ro 15-1788, a specific benzodiazepine antagonist would reverse the anxiolytic effect of VPA (200 mg/kg) in the Geller-Seifter paradigm was tested, using male albino rats. VPA (200 mg/kg) induced disinhibition which was antagonized by a convulsant benzodiazepine, Ro 5-3663 (1 mg/kg), but not by imidazobenzodiazepine, Ro 15-1788 at doses of 10 mg/kg, or 30 mg/kg. However, Ro 15-1788 (30 mg/kg) did have a short lasting antagonistic effect on VPA when tested in a "condensed" form (see text) of the conflict test. The nature of the anticonflict potency of VPA is discussed.

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A behavioral examination of convulsant benzodiazepine and GABA antagonist, Ro 5-3663, and benzodiazepine-receptor antagonist Ro 15-1788.

The potential "anxiogenic" effects of convulsant benzodiazepine and GABA-antagonist, Ro 5-3663 and specific antagonist of benzodiazepine receptors, Ro 15-1788 were compared in the Geller-Seifter conflict paradigm. Chlordiazepoxide (CDP) (5 mg/kg) was used as a "positive" control. Both Ro 5-3663 (1 mg/kg) and Ro 15-1788 (10 mg/kg) antagonized the anticonflict effect of CDP. However, while Ro 15-1788 had a modest anticonflict potency. Ro 5-3663 had an anxiogenic effect in its own right.

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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↗

The partial reinforcement extinction effect: influence of chlordiazepoxide in septal lesioned rats.

Rats sustained electrolytic lesions either in the medial septal (MS) or lateral septal (LS) area or they were sham-operated. They were tested in the straight alley with food reward on either continuous (CRF) or partial (PRF) reinforcement at one trial a day and were injected with either 5 mg/kg chlordiazepoxide HCl (CDP) or with saline before the daily trial throughout the acquisition and extinction. The effects of the drug on resistance to extinction interacted with those of the LS lesion in ways which were consistent with the hypothesis that CDP acts via the lateral septal area if it is injected during acquisition on a PRF schedule. MS lesions produced only small changes in the effects of CDP. In general, CDP acted to reverse the effects produced by each lesion: Under those conditions in which MS lesions produced faster running speeds, CDP caused the lesioned animals to run slower; and under those conditions in which LS lesions produced slower running speeds, CDP caused the lesioned animals to run faster.

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The effects of hippocampectomy and of fimbria section upon the partial reinforcement extinction effect in rats.

Rats were trained to run in an alley for food reward given on every trial (continuous reinforcement, CR) or on a random 50% of trials (partial reinforcement, PR) and were then extinguished. Sham-operated controls showed the usual partial reinforcement extinction effect (PREE), i.e., PR-trained animals were more resistant to extinction than CR-trained animals. The PREE was abolished by hippocampectomy, which increased resistance to extinction in CR-trained rats and decreased it in PR-trained rats. Bilateral fimbria section had no effect on resistance to extinction in either condition. These results are discussed in the light of theories of hippocampal function and the anatomy of septohippocampal connections.

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The effects of chlordiazepoxide HCl administration upon punishment and conditioned suppression in the rat.

Rats were trained to lever press for sucrose on a random interval (RI) 64-s schedule. During a 55 min session there were four 3 min "intrusion periods" signalled by a flashing house-light. In experiment 1 there were two groups matched for baseline response rate. During the intrusion periods one group received response-independent footshock on an independent RI 64 schedule; the other group received response-contingent shock on this schedule. Shock intensity was varied for each rat to match degree of response suppression between the two groups. Chlordiazepoxide HCl (CDP) in doses 0.5-5 mg/kg alleviated response suppression equally in both groups. Experiment II followed the same procedure, except that all animals had the same shock intensity, producing greater response suppression in the response-contingent shock groups. CDP alleviated response suppression more in the response-contingent shock groups, significantly so at 5 mg/kg, nonsignificantly at 1 mg/kg. These results suggest that previous reports that CDP differentially alleviates the response suppression produced by response-contingent shock are an artefact of rate dependency.

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Spontaneous alternation of body turns and place: differential effects of amylobarbitone, scopolamine and septal lesions.

Sodium amylobarbitone, scopolamine and septal and hippocampal lesions all reduce spontaneous alternation. However, septal lesions appear to reduce alternation of places more than body turns, while the reverse is true for hippocampal lesions. The present experiments tested the effects of amylobarbitone and scopolamine on place and body turn alternation. Medial and lateral septal lesions were also tested. The former block hippocampal theta rhythm but the latter do not. Amylobarbitone (20 mg/kg, IP) reduced alternation of body turns to chance levels when this was present in control animals, but it did not affect alternation of place. Scopolamine (1.2 mg/kg, IP) reduced both body turn alternation and place alternation. Medial septal lesions produced significant perseveration of body turns and produced a non-significant reduction in place alternation. Lateral septal lesions, tested in a small number of animals, did not appear to affect alternation. The treatments thus reduce spontaneous alternation in differing ways which can in part be accounted for in terms of their differing effects on hippocampal theta rhythm.

Amobarbital↗

Septo-hippocampal connections and the hippocampal theta rhythm.

Recordings were made of spontaneous hippocampal theta activity in free-moving rats, before and after a variety of lesions. Three recording sites were used to monitor activity in the dorsal hippocampus, the ventral hippocampus, or close to the site of the hippocampal flexure. Electrolytic lesions were made in the medial septal area or the dorso-lateral septal area; surgical transections were made of the fimbria or dorso-medial area of the fornix. Following lesions restricted to the medial septal area, theta was abolished throughout the hippocampus; after lesions restricted to the dorso-lateral septal area theta was retained. Fimbria lesions abolished it in the dorsal, but not the ventral, hippocampus. In some subjects the hippocampal formation was subsequently stained for cholinesterase: cholinesterase staining loss was generally associated with theta loss, but this was not clear at the flexure recording site. It was confirmed that theta is dependent upon the integrity of the medial septal area. It was concluded that damage to hippocampal afferents from the septum does abolish theta, while damaging the feedback efferents does not.

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Effect of runway training on rat brain tyrosine hydroxylase: differential effect of continuous and partial reinforcement schedules.

Previous experiments have implicated ascending noradrenergic systems in the development of the behavioural responses to different patterns of reward. In this report food deprived male Sprague--Dawley rats were trained to run a straight alley for good reward on a continuous reinforcement (CRF) or a partial reinforcement (PRF) schedule. Tyrosine hydroxylase measured in a partially solubilized preparation from hippocampus and hypothalamus at the end of acquisition was not different from controls, indicating that enzyme induction does not occur during either training schedules. However, hippocampal synaptosomal tyrosine hydroxylation rates from the CRF group was significantly higher than from either the PRF group or the handled controls. This indicates that at the end of the acquisition schedule the noradrenergic projection to hippocampus was more active in the CRF group than with the PRF group or the handled control.

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