Abstract
Behavioral control over a stressor limits the impact of the stressor being experienced and produces enduring changes that reduce the effects of future stressors. In rats, these stress-buffering effects of control (escapable stress, ES) require activation of the medial prefrontal cortex (mPFC) and prevent the typical amygdala-dependent behavioral outcomes of uncontrollable stress (inescapable stress, IS). Parvalbumin (PV) interneurons regulate output of excitatory neurons, and most mPFC PV neurons are surrounded by perineuronal nets (PNNs), which regulate firing. We exposed male rats to a single session of ES, IS, or no stress and measured c-Fos expression within PV/PNN-containing cells in mPFC subregions (prelimbic, PL; infralimbic, IL) and in the lateral amygdala. We also measured the number and intensity of PNNs. Within PL and IL PV/PNN cells, both ES and IS increased c-Fos intensity in PV/PNN, non-PV, and non-PNN cells. Within the IL, only ES increased the number of c-Fos-expressing PV/PNN-labeled cells. In the lateral amygdala, only ES increased c-Fos intensity within PV cells and PV/PNN cells. Thus, PV neurons in the IL and lateral amygdala may represent an important substrate by which behavioral control buffers against the amygdala-dependent behavioral outcomes typically observed after uncontrollable stress.
Published Version
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