Background. The consolidation of episodic memory is particularly vulnerable to fluctuations in glucocorticoid levels, both during wakefulness and during sleep. Corticosteroid exposure is associated with changes in endogenous glucocorticoid activity, sleep disruption, episodic memory impairment, and reduced hippocampal volume. This dissertation had two primary aims. The first was to explore the relationship between corticosteroid exposure and sleep-dependent memory processes, including dreaming, with special focus on associations between corticosteroid exposure and (a) night-time glucocorticoid activity and (b) sleep organization. The second was to explore the neuroanatomical foundation for these relationships in young adults with asthma. To achieve these aims, I conducted three studies. Methods. Study 1 (N = 68) used a cross-sectional, matched-sample, quasiexperimental design to compare night-time salivary cortisol levels, memory performance preand post-sleep, sleep organization (measured using polysomnography), and dreaming in groups of asthmatics and non-asthmatics with varying degrees of corticosteroid exposure. Study 2 (N = 23) used a double-blind, randomized placebo-control true experimental design to test, in healthy young adults, the effects of a single 25 mg dose of prednisone on the same outcome measures. Study 3 (N = 19) used a quasi-experimental design to compare hippocampal volume of moderate-to-high corticosteroid-exposed asthmatics with that of matched healthy controls. That study also examined the relationship between (a) night-time cortisol levels and hippocampal volume, (b) night-time cortisol levels and declarative memory performance, (c) hippocampal volume and declarative memory performance. All participants were English-speaking university students, aged 18-39 years. Results. Studies 1 and 2 showed that, relative to healthy controls, night-time glucocorticoid activity was elevated and sleep organization was disrupted in corticosteroidexposed individuals. Furthermore, there were significant inverse associations between glucocorticoid activity and (a) the organization of slow wave sleep (SWS) and rapid-eye movement (REM) sleep, (b) performance on both declarative and procedural memory tasks, and (c) the episodic memory content of dreams. There were significant positive associations between (a) the proportions and the organization of SWS and REM sleep and performance on measures of both declarative and procedural memory, and (b) the organization of REM sleep and the episodic content of dreams. Study 3 data analyses detected significantly smaller hippocampal volume in asthmatics relative to controls. Severity of asthma was inversely related to left hippocampal volume, but corticosteroid exposure alone was not. Furthermore, a smaller hippocampus was associated with better memory performance among healthy controls, but not among asthmatics. Conclusions. The association between the organization of SWS and REM sleep and performance on measures of both declarative and procedural memory lends support to the sequential hypothesis of sleep-dependent memory processing. The current findings also suggest that glucocorticoid activity is associated with (a) dream content, (b) the organization of SWS and REM sleep, and (c) post-sleep memory performance after sleep, and that these relationships may intersect. Although asthmatics did not display memory deficits or aberrant dreaming patterns, their hippocampal volume data, patterns of night-time cortisol, and sleep disruptions suggest further investigation is warranted into the implications of subtle HPA-axis dysfunction and consequent atypical brain development on cognitive function and quality of life in asthmatics, whether exposed to corticosteroid treatment or otherwise.