The persistence of acute restraint stress-induced anxiety-like behavior in rats: the glucocorticoids as modulators of the dendritic plasticity and the neuronal activity in the basolateral amygdala complex
Anxiety disorders generate a range of behavioral responses to danger triggered by innocuous and unpredictable stimuli. Both acute stress and elevated concentrations of glucocorticoid hormones (GCs) promote persistent anxiety-related behavior as well as increased density of dendritic spines in the basolateral amygdala complex (BLA) in rats. BLA is a key structure for fear behavior and anxiety. In fact, recent work from our group has shown a crucial role of the glucocorticoid receptor (GR) signaling in BLA for anxiety-related behavior expressed both immediately and late after acute restraint stress. However, it is unclear whether the morphological changes in the dendritic tree and in the activity of BLA neurons due to stress are events that depend directly on the genomic signaling of GC in this encephalic structure, as well as whether these biological changes are a sine qua non condition for the persistence of anxiety-like behavior. Therefore, the objective of this project is to investigate whether there is an interdependence between increased corticosterone signaling (CORT, main murine GC), via GR, and the events of remodeling of dendritic spines and alteration in neuronal activity in BLA, and if those are necessary for the manifestation of late anxiety-related behavior.
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