It suggests government departments and hospital administrators when formulating interventions to prevent work stress and occupational burnout. These interventions can subsequently prevent episodes of depression in paediatric intensive care unit nurses, thereby providing patients with a safe and high-quality nursing environment.

Adult rats with extensive, bilateral neurotoxic lesions of the hippocampus showed normal forgetting curves for object recognition memory, yet were impaired on closely related tests of object recency memory. The present findings point to specific mechanisms for temporal order information (recency) that are dependent on the hippocampus and do not involve object recognition memory. The object recognition tests measured rats exploring simultaneously presented objects, one novel and the other familiar. Task difficulty was varied by altering the retention delays after presentation of the familiar object, so creating a forgetting curve. Hippocampal lesions had no apparent effect, despite using an apparatus (bow-tie maze) where it was possible to give lists of objects that might be expected to increase stimulus interference. In contrast, the same hippocampal lesions impaired the normal preference for an older (less recent) familiar object over a more recent, familiar object. A correlation was found between the loss of septal hippocampal tissue and this impairment in recency memory. The dissociation in the present study between recognition memory (spared) and recency memory (impaired) was unusually compelling, because it was possible to test the same objects for both forms of memory within the same session and within the same apparatus. The object recency deficit is of additional interest as it provides an example of a nonspatial memory deficit following hippocampal damage.

Within-subjects procedures with rats assessed the associative structures acquired during conditioning trials in which the interval between the stimuli and food was either short or long (i.e., A-10 s→food and B-40 s→food). In Experiments 1 and 2, after these conditioning trials, A and B served as second-order reinforcers for 2 further stimuli (i.e., X→A and Y→B); whereas Experiment 3 used a sensory preconditioning procedure in which X→A and Y→B trials occurred before the conditioning trials, and rats were finally tested with X and Y. In each experiment, Y elicited greater responding at test than did X. This finding supports the contention that the long-lived trace of B (associated with food on B-40 s→food trials) is more similar to the memory of B that was associatively provoked by Y, than is the short-lived trace of A (associated with food on A-10 s→food trials) to the memory of A that was associatively provoked by X. These conclusions were reinforced by the effects of a neural manipulation that disrupted discrimination learning involving the short traces of stimuli but not the long traces of the same stimuli.

The biological basis of the increased risk for psychiatric disorders seen in 15q11.2 copy number deletion is unknown. Previous work has shown disturbances in white matter tracts in human carriers of the deletion. Here, in a novel rat model, we recapitulated low dosage of the candidate risk gene CYFIP1 present within the 15q11.2 interval. Using diffusion tensor imaging, we first showed extensive white matter changes in Cyfip1 mutant rats, which were most pronounced in the corpus callosum and external capsule. Transmission electron microscopy showed that these changes were associated with thinning of the myelin sheath in the corpus callosum. Myelin thinning was independent of changes in axon number or diameter but was associated with effects on mature oligodendrocytes, including aberrant intracellular distribution of myelin basic protein. Finally, we demonstrated effects on cognitive phenotypes sensitive to both disruptions in myelin and callosal circuitry.

Two experiments examined the content of configural learning in rats. In Experiment 1, after simple pre-exposure to two hybrid contexts (AB and CD), rats acquired a configural discrimination involving two of the contexts (A and C) and two auditory stimuli (X and Y; AX→food, AY→no food, CX→no food, and CY→food). When rats were then placed in context B, they were more likely to respond to X than Y, and when they were placed in context D the reverse was the case. Experiment 2 demonstrated that rats can acquire a configural discrimination involving the presence of context (A) and its memory trace (a; AX→food, AY→no food, aX→no food, and aY→food). These results show that associatively provoked memories (Experiment 1) and memory traces (Experiment 2) can participate in configural discriminations.