It has been proposed that a brief exposure to stress leads to deficits in fear memory extinction, and enhances glutamate transmission in the prefrontal cortex (PFC). The PFC is an important site involved in cardiovascular, neuroendocrine and behavioral responses. Furthermore, there is a high expression of glucocorticoids (GRs) and mineralocorticoids (MRs) receptors in this brain structure. In ours previous results, we showed that a brief and single stress episode prior to contextual fear conditioning promotes extinction deficit. Also, our data demonstrated that GRs in ventromedial region of the PFC (vmPFC) are necessary for the impairing extinction memory promoted by acute stress, maybe influencing the glutamatergic transmission and plasticity. However, further evidence is still necessary to completely understand the memory extinction process under stress conditions. Now, our objective is evaluation of the long-term effect of acute stress on the fear extinction memory, more specifically, the morphological and molecular mechanisms triggered by acute stress, involving the glucocorticoids and mineralocorticoids receptors in the prefrontal cortex in this cognitive process. Our hypothesis is that the acute stress promotes deficit in the contextual fear extinction through alterations in the expression of the GRs and MRs in the vmPFC which results in abnormal glutamatergic transmission, as well the morphological changes in this brain area.
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