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D B Sternberg

Publications and source records attributed to D B Sternberg.

13 recordsLinked to original sources
PubMed1986

Epinephrine-induced memory facilitation: attenuation by adrenoceptor antagonists.

The present study examined the relative importance of alpha- and beta-adrenoceptors in the memory modulatory effects of epinephrine. Posttraining epinephrine administration enhanced retention performance of a one-trial inhibitory avoidance response. Further pretraining injections of a variety of adrenoceptor antagonists, including selective alpha 1-, alpha 2-, beta 1- and/or beta 2-adrenoceptor antagonists, attenuated the retention enhancing effects of posttraining epinephrine. These results suggest that alpha- and beta-adrenoceptors of both subtypes are involved in the memory-modulating effects of epinephrine.

Adrenergic alpha-Antagonists↗
PubMed1985

Noradrenergic changes and memory loss in aged mice.

The present paper addresses the question of whether a decline of central noradrenergic activity is associated with aging and memory loss in mice. Receptor binding techniques were utilized to compare alpha 2-adrenoceptor density in the brains of aged and young mice. Using [3H]rauwolscine, a selective alpha 2-adrenoceptor antagonist, two membrane binding sites were identified which were differentially affected by age. Whereas the density of high-affinity binding sites was unchanged in aged brain as compared to young controls, there was a significant decrease in the number of low-affinity sites. In a separate study, animals were tested for performance on a step-through inhibitory avoidance task, prior to sacrifice and morphological analysis of the brainstem noradrenergic nucleus locus coeruleus (LC). Aged mice exhibited a significant decrease in task retention as compared to young controls; a small, though non-significant, decline was also observed in the numbers of cells within LC. While young mice exhibited low within-group variance, individual aged animals differed greatly in both LC cell number and behavioral performance. Within the aged population, there was a highly significant correlation between the extent of LC cell loss and the degree of memory impairment. These results provide further evidence for an age-related decline in central noradrenergic function which may contribute to an associated memory loss.

Aging↗
PubMed1985

Epinephrine facilitation of appetitive learning: attenuation with adrenergic receptor antagonists.

Previous studies using aversive training tasks have reported that retention is enhanced by post-training administration of epinephrine. This study investigated the effects of post-training administration of epinephrine on retention of an appetitive task. The results indicate that epinephrine can enhance retention performance in an appetitive task of both rats and mice. Pretraining injections of propranolol and phenoxybenzamine, alpha- and beta-adrenergic receptor antagonists, attenuate the memory-enhancing effects of epinephrine. These results are consistent with the view that release of peripheral epinephrine may regulate storage of new information and may mediate memory modulation produced by a variety of treatments.

Animals↗
PubMed1985

Epinephrine-induced learning under anesthesia: retention performance at several training-testing intervals.

While under deep barbiturate anesthesia, rats received a series of 10 classical conditioning trials in which white noise was paired with intramuscular shock. The anesthetized animals received either saline or epinephrine injections prior to the training trials. Independent sets of animals were tested for retention performance 2, 7, or 15 days after training. In these test trials, a conditioned suppression measure was used in which the white noise was turned on while the animals were drinking. The results indicated that the animals that had received saline while trained under anesthesia exhibited no evidence of later retention. Animals that had received epinephrine injections prior to training under anesthesia suppressed their drinking in the presence of the white noise when tested 2 or 7, but not 15, days later. Thus, the results indicate that epinephrine can enable learning under anesthesia and, in addition, forgetting occurs within 15 days.

Anesthesia↗
PubMed1984

Epinephrine enables Pavlovian fear conditioning under anesthesia.

Rats under Pavlovian defensive conditioning (noise paired with shock) while under general anesthesia. Peripheral administration of epinephrine (0.01 to 1.0 milligram per kilogram of body weight) during training resulted in the acquisition of conditioned fear, as shown 10 days later by conditioned suppression of water drinking. Analysis of heart rate and measurement of reflexes during training indicated that epinephrine did not lighten the state of anesthesia. These results indicate that epinephrine enables the learning of conditioned fear in the anesthetized brain.

Anesthesia, General↗
PubMed1983

Memory facilitation and impairment with supraseizure electrical brain stimulation: attenuation with pretrial propranolol injections.

Post-training supraseizure stimulation of frontal cortex enhances retention of active avoidance in rats trained using a low footshock but impairs retention when high footshock is used in training. Pretreatment with the adrenergic antagonist propranolol results in attenuation of both memory facilitation and amnesia. These results are consistent with previous evidence indicating that adrenergic antagonists attenuate amnesia and facilitation produced by a variety of agents and suggest that memory modulatory treatments may enhance or impair memory by actions which include effects on adrenergic systems.

Adrenergic Fibers↗
PubMed1983

4-OH amphetamine enhances retention of an active avoidance response in rats and decreases regional brain concentrations of norepinephrine and dopamine.

An .82 mg/kg dose of dl-4-OH amphetamine administered ip immediately following training in a one-way active avoidance task enhanced retention performance measured 24 hr later. In contrast, 4-OH amphetamine in a dose range of .41--1.65 mg/kg ip did not affect retention of a swim escape task. The behaviorally active dose of .82 mg/kg 4-OH amphetamine decreased dopamine concentrations in the amygdala and hippocampus. A dose of 8.2 mg/kg 4-OH amphetamine administered ip to naive untrained rats decreased concentrations of norepinephrine measured in the amygdala, cortex, hippocampus, hypothalamus, and midbrain; decreased concentrations of dopamine in the amygdala, cortex, hippocampus, and striatum; and significantly reduced concentrations of norepinephrine and epinephrine in the adrenal medulla. In addition, because the integrity of the adrenal medulla is necessary for the enhancing action of 4-OH amphetamine and because 4-OH amphetamine reduces concentrations of catecholamines in the brain and adrenal medulla, it is possible that 4-OH amphetamine affects retention performance by a dual action on the brain and the adrenal medulla.

Adrenal Medulla↗
PubMed1981

Retrograde amnesia produced by electrical stimulation of the amygdala: attenuation with adrenergic antagonists.

Subseizure electrical stimulation of the amygdala produced retrograde amnesia for a visual discrimination shock-motivated task. Animals pretreated with the alpha-adrenergic antagonist phenoxybenzamine, or the beta-adrenergic antagonist propranolol, did not develop amnesia. The findings indicate that adrenergic antagonists attenuate amnesia produced by amygdala stimulation for visual discrimination training. These results are consistent with previous evidence indicating that adrenergic antagonists attenuate the amnesias produced by a variety of agents, and thus, suggest that adrenergic mechanisms may be involved in the production of retrograde amnesia.

Amnesia↗
PubMed1978

Retrograde amnesia produced by several treatments: evidence for a common neurobiological mechanism.

This experiment examined the effects on memory of various amnestic treatments in animals earlier treated with the alpha-adrenergic antagonist phenoxybenzamine (PBZ). Thirty minutes before being trained in a one-trial inhibitory (passive) avoidance task, animals received an injection of PBZ or saline. Immediately after training, each animal received one of the following amnestic treatments: stimulation of the frontal cortex or amygdala, pentylenetetrazol, diethyldithiocarbamate, or cycloheximide. In control animals, each treatment produced retrograde amnesia. However, PBZ-treated animals did not develop amnesia. These findings suggest that there may be a common neurobiological mechanism underlying the amnesias produced by many treatments.

Amnesia↗