Abstract
Chronic stress is a risk factor for the development of psychiatric disorders, some of which involve dysfunction of the prefrontal cortex (PFC). There is a higher prevalence of these chronic stress-related psychiatric disorders during adolescence, when the PFC has not yet fully matured. In the present work we studied the effect of repeated stress during adolescence on synaptic function in the PFC in adolescence and adulthood. To this end, adolescent Sprague-Dawley rats were subjected to seven consecutive days of restraint stress. Afterward, both synaptic transmission and short- and long-term synaptic plasticity were evaluated in layer 1 of medial-PFC (mPFC) slices from adolescent and adult rats. We found that repeated stress significantly reduced the amplitude of evoked field excitatory post-synaptic potential (fEPSP) in the mPFC. Isolation of excitatory transmission reveled that lower-amplitude fEPSPs were associated with a reduction in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated transmission. We also found that repeated stress significantly decreased long-term depression (LTD). Interestingly, AMPA/kainate receptor-mediated transmission and LTD were recovered in adult animals that experienced a three-week stress-free recovery period. The data indicates that the changes in synaptic transmission and plasticity in the mPFC induced by repeated stress during adolescence are reversed in adulthood after a stress-free period.
Highlights
Stress is a biological response that allows adaptation to environmental threats (Rodrigues et al, 2009)
Our results indicate that the repeated stress-induced decrease in basal synaptic transmission during adolescence is mediated by post-synaptic alterations in amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate dependent transmission, but not because of alterations in GABAA or NMDA receptors
We previously found that repeated stress during adolescence impairs the recall of the extinction of conditioned fear, an impairment that was reversed in adulthood (Negrón-Oyarzo et al, 2014)
Summary
Stress is a biological response that allows adaptation to environmental threats (Rodrigues et al, 2009). The prefrontal cortex (PFC), a brain region involved in controlling high-level executive functions (Fuster, 2001; Miller and Cohen, 2001), displays functional chronic stress and synaptic plasticity in PFC impairment in patients suffering mood disorders (Drevets et al, 1997; Johnstone et al, 2007). This suggests that chronic stress induces alterations in the PFC related to behavioral dysfunction (Liston et al, 2006; Miracle et al, 2006; Dias-Ferreira et al, 2009; Holmes and Wellman, 2009)
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