Evidence reviewed here suggests that many treatments that retroactively enhance or impair memory in rats and mice may act by releasing epinephrine from the adrenal medulla: (1) When administered shortly after training, epinephrine injections modulate memory storage processes; (2) plasma epinephrine levels assessed shortly after training predict later performance of learned responses in several situations; and furthermore, (3) peripherally administered adrenergic antagonists block the effects on memory of epinephrine and of many other treatments that enhance and impair memory. In addition, the rapid forgetting exhibited by juvenile and aged rodents can be retarded (i.e., memory is improved) by posttraining epinephrine injections, suggesting that age-related memory deficits may reflect inadequate functions of those neuroendocrine systems responsible, in part, for regulating memory storage. These results, together with the additional finding that epinephrine enhances the establishment of a neurophysiological analogue of memory, long-term potentiation, suggest that the hormone regulates neurobiological processes responsible for memory formation.
94Evidence accumulated over the past 25 years indicates that, if administered soon after a training experience, a variety of treatments can retroactively modify memorystorage processing (Gold & Zometzer, 1983;McGaugh, 1966;McGaugh & Herz, 1972). Amnestic agents used in the past have included electroconvulsive shock, localized electrical stimulation of the brain, and drugs that interfere with protein synthesis, neurotransmitter synthesis, or neurotransmitter function. When considered with the finding that retrograde amnesia can be observed after training in a wide range of behavioral tasks and in a large number of species, two features are clear. First, if a treatment produces amnesia in one task or in one species, that treatment is likely to do so in other tasks and other species. Second, although the specific time course may vary widely under different conditions, the treatments produce more severe memory disruption when administered soon after training than they do when administered at long delays after training. Similarly, many studies provide evidence that some treatments, including administration of such stimulant drugs as amphetamine and low doses of pentylenetetrazol, can enhance the storage of recent information. Here again, the treatments have the largest effects on memory when administered at short intervals after training. The generality of these findings, in terms of task, species, and time-dependency, suggests some biological commonalities in the mechanisms by which most treatments modulate memory-storage processes under a broad spectrum of specific experimental conditions. A