PubMed Health⌕ Search

Biomedical subjects

Tracey J Shors

Publications and source records attributed to Tracey J Shors.

24 records · Page 2Linked to original sources
PubMed2003

Glucocorticoids are necessary for enhancing the acquisition of associative memories after acute stressful experience.

Exposure to acute stressful experience can enhance the later ability to acquire new memories about associations between stimuli. This enhanced learning is observed during classical eyeblink conditioning of both hippocampal-dependent and -independent learning. It can be induced within minutes of the stressful event and persists for days. Here we examined the role of the major stress hormones glucocorticoids in the enhancement of learning after stress. In the first two experiments, it was determined that adrenalectomy (ADX), with and without replacement of basal levels of corticosterone, prevented the stress-induced enhancement of trace conditioning, a task that is dependent on the hippocampus for acquisition. In a third experiment, demedullation, which removes the adrenal medulla but leaves the adrenal cortex and corticosterone levels intact, did not affect the enhancement of learning after stress. In a fourth experiment, ADX prevented the stress-induced enhancement of delay conditioning, a hippocampal-independent task. In a final experiment, it was determined that one injection of stress levels of corticosterone enhanced new learning within minutes but not new learning 24 h later. Together these results suggest that endogenous glucocorticoids are necessary and sufficient for transiently enhancing acquisition of new associative memories and necessary but insufficient for persistently enhancing their acquisition after exposure to an acute stressful experience.

Acute Disease↗
PubMed2003

Estrogen-mediated effects on depression and memory formation in females.

Women are twice as likely to suffer from depression as men. It has been proposed that the ovarian hormones estrogen and progesterone contribute to the higher incidence of this potentially debilitating disorder. Depression can also be accompanied by a loss of cognitive performance. Here we review estrogen-mediated effects on depression and memory formation in females. We propose that changes in levels of estrogen are associated with sex differences in learning as well as changes in affect prior to menses, immediately after pregnancy and during perimenopause and the menopausal transition. Finally, we discuss the animal model of depression known as 'learned helplessness' and describe research from our laboratory demonstrating that exposure to an acute stressful experience compromises a female's later ability to acquire certain types of new memories. This response to stressful experience is opposite to that observed in males and is dependent on the presence of estrogen, and more specifically-changing levels of estrogen. This observation indicates that females and males can use different hormonal and neural mechanisms to respond to the same emotional event and underscore the importance of studying the unique and changing biology of females, especially when considering treatment strategies for depression and stress-related illness.

Animals↗
PubMed2002

Testosterone in utero and at birth dictates how stressful experience will affect learning in adulthood.

Exposure to an acute stressful event can enhance learning in male rats, whereas exposure to the same event dramatically impairs performance in females. Here we tested whether the presence of sex hormones during early development organizes these opposite effects of stress on learning in males vs. females. In the first experiment, males were castrated at birth whereas females were injected with testosterone. Rats were trained as adults on the hippocampal-dependent learning task of trace eyeblink conditioning. Performance in adult males that had been castrated at birth was still enhanced by exposure to an acute stressful experience. However, adult females injected with testosterone at birth responded in the opposite direction, i.e., exposure to the stressor that typically reduces performance instead enhanced their levels of conditioning. In the second experiment, exposure to testosterone was manipulated in utero by injecting pregnant females with a testosterone antagonist. After foster rearing, adult offspring were exposed to the stressor and trained on the hippocampal-dependent learning task of trace conditioning. Although performance in adult females was unaffected by antagonizing testosterone in utero, i.e., stress still reduced performance, the enhancement of conditioning after stress in adult males was prevented. Thus, the presence of sex hormones during gestation and development organizes whether and how acute stressful experience will affect the ability to acquire new information in adulthood. As with many sexual behaviors, these cognitive responses to stress appear to be masculinized by exposure to testosterone and feminized by its absence during very early development.

Animals↗
PubMed2002

Neurogenesis may relate to some but not all types of hippocampal-dependent learning.

The hippocampal formation generates new neurons throughout adulthood. Recent studies indicate that these cells possess the morphology and physiological properties of more established neurons. However, the function of adult generated neurons is still a matter of debate. We previously demonstrated that certain forms of associative learning can enhance the survival of new neurons and a reduction in neurogenesis coincides with impaired learning of the hippocampal-dependent task of trace eyeblink conditioning. Using the toxin methylazoxymethanol acetate (MAM) for proliferating cells, we tested whether reduction of neurogenesis affected learning and performance associated with different hippocampal dependent tasks: spatial navigation learning in a Morris water maze, fear responses to context and an explicit cue after training with a trace fear paradigm. We also examined exploratory behavior in an elevated plus maze. Rats were injected with MAM (7 mg/kg) or saline for 14 days, concurrent with BrdU, to label new neurons on days 10, 12, and 14. After treatment, groups of rats were tested in the various tasks. A significant reduction in new neurons in the adult hippocampus was associated with impaired performance in some tasks, but not with others. Specifically, treatment with the antimitotic agent reduced the amount of fear acquired after exposure to a trace fear conditioning paradigm but did not affect contextual fear conditioning or spatial navigation learning in the Morris water maze. Nor did MAM treatment affect exploration in the elevated plus maze. These results combined with previous ones suggest that neurogenesis may be associated with the formation of some but not all types of hippocampal-dependent memories.

Animals↗
PubMedDate not supplied

Learning during stressful times.

Stressful life events can have profound effects on our cognitive and motor abilities, from those that could be construed as adaptive to those not so. In this review, I discuss the general notion that acute stressful experience necessarily impairs our abilities to learn and remember. The effects of stress on operant conditioning, that is, learned helplessness, as well as those on classical conditioning procedures are discussed in the context of performance and adaptation. Studies indicating sex differences in learning during stressful times are discussed, as are those attributing different responses to the existence of multiple memory systems and nonlinear relationships. The intent of this review is to highlight the apparent plasticity of the stress response, how it might have evolved to affect both performance and learning processes, and the potential problems with interpreting stress effects on learning as either good or bad. An appreciation for its plasticity may provide new avenues for investigating its underlying neuronal mechanisms.

Adaptation, Psychological↗