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Abstract
BackgroundAdolescent social stress is associated with increased incidence of mental illnesses in adulthood that are characterized by deficits in cognitive focus and flexibility. Such enhanced vulnerability may be due to psychosocial stress-induced disruption of the developing mesocortical dopamine system, which plays a fundamental role in facilitating complex cognitive processes such as spatial working memory. Adolescent rats exposed to repeated social defeat as a model of social stress develop dopaminergic hypofunction in the medial prefrontal cortex as adults. To evaluate a direct link between adolescent social stress and later deficits in cognitive function, the present study tested the effects of adolescent social defeat on two separate tests of spatial working memory performance.MethodsAdult rats exposed to adolescent social defeat and their controls were trained on either the delayed win-shift task or the delayed alternating T-Maze task and then challenged with various delay periods. To evaluate potential differences in motivation for the food reward used in memory tasks, consumption and conditioned place preference for sweetened condensed milk were tested in a separate cohort of previously defeated rats and controls.ResultsCompared to controls, adult rats defeated in adolescence showed a delay-dependent deficit in spatial working memory performance, committing more errors at a 90 s and 5 min delay period on the T-maze and win-shift tasks, respectively. Observed memory deficits were likely independent of differences in reward motivation, as conditioned place preference for the palatable food used on both tasks was similar between the adolescent social defeat group and control.ConclusionsThe results demonstrate that severe social stressors during adolescence can produce long term deficits in aspects of cognitive function. Given the dependence of spatial working memory on prefrontal dopamine, pharmacologically reversing dopaminergic deficiencies caused by adolescent social stress has the potential to treat such cognitive deficits.
Highlights
Adolescent social stress is associated with increased incidence of mental illnesses in adulthood that are characterized by deficits in cognitive focus and flexibility
In terms of preference for cues associated with sweetened condensed milk (SCM) reward in adulthood, analysis of the Conditioned place preference (CPP) test session following conditioning revealed that the ratio of time spent in the SCM-paired compartment compared to the non-SCM compartment did not differ between rats defeated in adolescence and control groups (F(1,14) = 0.610, p = 0.448; Figure 2)
While previously defeated rats showed impairment in delayed working memory performance that may be due to deficits in medial prefrontal cortex (PFC) (mPFC) DA, it is possible that differences in hippocampal monoaminergic activity caused by adolescent defeat [18] promoted enhanced utilization of spatial strategies to acquire the task initially during training. These experiments add to an ever growing body of literature in both in humans and animals reporting an adverse effect of stressors during childhood and adolescence on later cognitive function [15,35,36,37,61,62,63], which appears to relate to the vulnerability of the developing PFC to stress-induced disruption, by social stress [14,18,21,64]
Summary
Adolescent social stress is associated with increased incidence of mental illnesses in adulthood that are characterized by deficits in cognitive focus and flexibility. Structural variations in the PFC appear to mediate the relationship between early life stressors and later spatial working memory deficits [16], suggesting that early life stressors may alter the structure of the developing PFC to contribute to cognitive dysfunction later in life While such studies provide important retrospective data on the potential consequences of early life stressors on cognitive ability, the direct effects of adolescent social stress on executive function and its underlying neural mechanisms have yet to be explored
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