RESUMO
Stress-induced glucocorticoids can dampen learning and spatial memory via neuronal damage to the hippocampus. Cognition losses can be transient (associated with acute stress episodes) or permanent as in aged individuals who show chronic glucocorticoid-induced accelerated brain aging and neurodegeneration (dementia). Thus, chronic versus acute stress effects on spatial memory responses of quail selected for reduced (low stress, LS) or exaggerated (high stress, HS) plasma corticosterone (B) response to brief restraint were assessed. Aged food-motivated male LS and HS quail were tested for 10 min in a feed-baited 8-arm radial arm maze (RAM) 1) at 255 d of age (quail who had experienced lifelong management stressors but who were otherwise never intentionally stressed; that is, chronically stressed birds), 2) on the next day post-acute stressor treatment (5 min of restraint), and 3) on the next day without treatment (acute stress recovery). The RAM tests used the win-shift procedure in which visited arms were not rebaited. Radial arm maze performance was measured by determination of the total number of arm choices made, the number of correct entries made into baited arms out of the first 8 choices, the time required to make a choice, and the number of pellets eaten. Line effects (P < 0.001 in all cases) were detected for total number of arm choices made (HS < LS), number of correct entries made into baited arms out of the first 8 choices (HS < LS), time required to make a choice (HS > LS), and number of pellets eaten (HS < LS). However, neither the effects of day of RAM testing nor its interaction with line further influenced these variables. Thus, although selection for divergent plasma B responsiveness to an acute stressor was found to be associated with severe impairment of spatial memory in aged male HS compared with LS quail, the observed spatial memory impairments (HS > LS) could not be further altered by acute stressor treatment. Line differences in cognition may reflect lifelong management-induced stress episodes that periodically produce higher plasma B responses in HS than LS quail, which underlie HS quail memory deficits, or other etiologies, or both.
