together, these findings suggest that the brain compensates for negative effects of sleep deprivation on the hippocampal memory system by promoting the use of a striatal memory system. However, effects of sleep deprivation can still appear later on because the alternative learning mechanisms and brain regions involved may result in reduced flexibility under conditions requiring adaptation of previously formed memories.

Stress and sleep are related to each other in a bidirectional way. If on one hand poor or inadequate sleep exacerbates emotional, behavioral, and stress-related responses, on the other hand acute stress induces sleep rebound, most likely as a way to cope with the adverse stimuli. Chronic, as opposed to acute, stress impairs sleep and has been claimed to be one of the triggering factors of emotional-related sleep disorders, such as insomnia, depressive- and anxiety-disorders. These outcomes are dependent on individual psychobiological characteristics, conferring even more complexity to the stress-sleep relationship. Its neurobiology has only recently begun to be explored, through animal models, which are also valuable for the development of potential therapeutic agents and preventive actions. This review seeks to present data on the effects of stress on sleep and the different approaches used to study this relationship as well as possible neurobiological underpinnings and mechanisms involved. The results of numerous studies in humans and animals indicate that increased sleep, especially the rapid eye movement phase, following a stressful situation is an important adaptive behavior for recovery. However, this endogenous advantage appears to be impaired in human beings and rodent strains that exhibit high levels of anxiety and anxiety-like behavior.

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Activation of the hypothalamic-pituitary-adrenal (HPA) axis is observed immediately after 96 h of paradoxical sleep (PS) deprivation. However, when individually or group PS-deprived rats are challenged with a mild stressor, they exhibit a facilitation of the corticosterone response, and a faster return to basal levels than control rats. Because the housing condition influences coping behaviour, we tested whether the type of PS deprivation (individually or in group) influenced anxiety-like behaviour in the elevated plus-maze and the accompanying adrenocorticotropin (ACTH) and corticosterone responses. Individually (I-DEP) or group deprived (G-DEP) rats and their appropriate control groups were either killed immediately after 96 h of sleep deprivation (time-point 0 or 'basal') or exposed to a 5-min test on the elevated plus maze and sampled 5, 20 or 60 min after test onset. Control of I-DEP rats showed reduced locomotor activity and augmented anxiety-like behaviour, replicating the effects of social isolation. Although I-DEP rats exhibited higher motor activity than cage control rats, these groups did not differ in regard to the percentage of entry and time spent in the open arms. G-DEP rats, in turn, ambulated more, entered and remained longer in the open arms, exhibiting less anxiety-like behaviour. PS-deprived rats exhibited higher ACTH and corticosterone 'basal' secretion than control rats. For all groups, peak ACTH secretion was reached at the 5-min time-point, returning to unstressed basal levels 60 min after the test, except for G-DEP rats, which showed a return at 20 min. Peak levels of corticosterone occurred at 5 min for PS-deprived groups and at 20 min for control groups. G-DEP rats showed a return to 'basal' unstressed levels at 20 min, whereas the I-DEP and control groups did so at 60 min. A negative correlation between exploration in the open arms and hormone concentrations was observed. These data indicate that housing condition influences the subsequent behaviour of PS-deprived rats in the EPM which, in turn, seems to determine the secretion profile of ACTH and corticosterone in response to the test.

Our results suggest that glucocorticoids do not mediate memory impairments but might be responsible for the weight loss induced by paradoxical sleep deprivation.