The effect of dexamethasone blockade of ACTH release on avoidance learning

Kasper-Pandi, Phyllis; Hansing, Ruth; Usher, David R.

doi:10.1016/0031-9384(70)90111-3

Cited by 16 publications

(8 citation statements)

References 17 publications

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“…The poor avoidance performance of subjects given DEX prior to training does not appear to result from a failure to acquire the problem or from DEX's acting as a state-dependent agent (see Pappas & Gray, 1971) because subjects given DEX prior to training, but not extinguished, had significantly higher retention scores than subjects given DEX prior to training and extinction and saline ( U = 16, p < .05) or ACTH ( U = 8.5, p < .02) prior to test. These data are in agreement with the findings of Kasper-Pandi et al (1970) in which pretreatment with DEX did not significantly impair acquisition of a one-way avoidance response. It was not necessary to include a saline-no-extinction condition in the present study as our concern was not with a possible disruption in acquisition by the DEX treatment.…”

Section: Resultssupporting

confidence: 92%

“…All injections were given in a volume of 1 ml per kilogram of body weight. Dexamethasone prior to training should reduce or block release of endogeneous ACTH in response to the aversive footshock employed in conditioning, as Kasper-Pandi et al (1970) showed this dose to be effective in shutting down the stress response of the pituitary-adrenal system of the rat to shock. Thus, ACTH should not be a component of the training memory for subjects given DEX prior to training but should be represented in the training memory of control subjects given saline.…”

Section: Methodsmentioning

confidence: 99%

“…One possible approach to decreasing the likelihood of endogenous ACTH's being a part of the training memory would be to block release of ACTH at training. Several previous studies have shown that administration of dexamethasone (DEX), a synthetic glucocorticoid, prior to presentation of an aversive stimulus effectively suppresses (via negative feedback) the release of endogenous ACTH (Beatty, Beatty, Bowman, & Gilchrist, 1970; Kasper-Pandi, Hansing, & Usher, 1970; Mormede & Dantzer, 1977; Pappas & Gray, 1971). So, in animals given DEX prior to avoidance training, ACTH should not be a component of the original training memory.…”

mentioning

confidence: 99%

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Administration of dexamethasone prior to training blocks ACTH-induced recovery of an extinguished avoidance response.

Ahlers¹,

Richardson²

1985

Behavioral Neuroscience

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Pretest administration of ACTH has been shown to produce recovery of an extinguished avoidance response. Presumably this effect is found because endogenous ACTH is a component of the original training memory. However, another possible explanation of this finding is that administration of the peptide acts as a novel stimulus that "disinhibits" the extinguished response. In order to test this "disinhibitory" hypothesis of ACTH-induced recovery of an extinguished avoidance response, some subjects were given dexamethasone 2 hr prior to training and extinction. This synthetic glucocorticoid is effective in blocking endogenous release of ACTH. Thus, ACTH should not be a component of the training memory in subjects given dexamethasone prior to training and extinction but would be a relatively novel stimulus condition at testing. Pretest administration of ACTH was found to be effective in alleviating performance deficits induced by extinction only for subjects given saline prior to training and extinction. Administration of ACTH had no effect on the avoidance responding of subjects given dexamethasone. These findings suggest that pretest administration of ACTH affects retrieval processes rather than acts as a disinhibitor.

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Section: Resultssupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Administration of dexamethasone prior to training blocks ACTH-induced recovery of an extinguished avoidance response.

Ahlers¹,

Richardson²

1985

Behavioral Neuroscience

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“…dexamethasone sodium phosphate (Decadron, Merck Sharp & Dohme, West Point, PA) 2 hr before passive avoidance training. This dose and time interval was selected on the basis of a previously published report that indicated significant suppression of ACTH release (Kasper-Pandi et al, 1970). Dexamethasone was mixed with 0.9% saline to produce an injection volume of 1 ml/kg.…”

Section: Methodsmentioning

confidence: 99%

Role of ACTH in recovery from retrograde amnesia induced by hypothermia in rats.

Santucci¹,

Riccio²,

Treichler³

1989

Behavioral Neuroscience

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The present investigation assessed whether increased congruency between ACTH state present shortly after training and that at testing contributed to memory recovery. If recovery were related to an increased correspondence between internal state present after training and that at testing, then suppressing ACTH release should block memory recovery. This was the hypothesis that was examined in the present investigation. Specifically, animals were trained on a passive avoidance task, administered hypothermia (the amnestic agent) and, shortly prior to testing, given treatments known to be effective in reversing memory loss induced by hypothermia. Before training (Experiment 1) or testing (Experiment 2) animals were injected with either dexamethasone (an agent that suppresses ACTH release) or saline. Results, in general, indicated that when ACTH release was suppressed, a blunted recovery effect was obtained. This reduction in the extent of memory recovery was observed when ACTH was suppressed either at training or at testing. These data are interpreted as providing support for an ACTH-related, state-dependent retention mechanism contributing to recovery from hypothermia-induced retrograde amnesia in rats.

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“…Avoidance extinction was delayed by ACTH independently of glucocorticoid production ( Bohus and Lissak, 1968;Levine, 1968;Guth et al, 1971). By contrast, corticosterone Conner and Levine, 1969), but not dexamethasone (Kasper-Pandi et al, 1970), was shown to have opposite effects on both acquisition and extinction of an avoidance response. The interaction of CRF, ACTH, and glucocorticoids with behavioral parameters is important when considering basal HPA axis activity and the avoidance score of some rat lines such as the Roman or the Syracuse High-and Low-Avoidance rats.…”

Section: Neuroendocrine Metabolie and Behavioral Responsesmentioning

confidence: 99%

Genetically Defined Animal Models of Neurobehavioral Dysfunctions

Driscoll¹

1992

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The effect of dexamethasone blockade of ACTH release on avoidance learning

Cited by 16 publications

References 17 publications

Administration of dexamethasone prior to training blocks ACTH-induced recovery of an extinguished avoidance response.

Administration of dexamethasone prior to training blocks ACTH-induced recovery of an extinguished avoidance response.

Role of ACTH in recovery from retrograde amnesia induced by hypothermia in rats.

Genetically Defined Animal Models of Neurobehavioral Dysfunctions

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