Norepinephrine mediates behavioral responses to stressors causing heightened vigilance and goal directed behaviors. However, following chronic stress individuals show enhanced impulsivity, fear, and anxiety. These behavioral responses are mediated by norepinephrine release in specific limbic brain areas and indicate chronic stress results in sensitized adrenergic receptor signaling. The present study aims to examine how chronic stress affects G protein-coupled receptor kinase-2 (GRK-2) in the bed nucleus stria terminalis (BNST) and prefrontal cortex (PFC). GRK-2 functions as an intracellular brake on adrenergic receptor signaling by decoupling adrenergic receptors from intracellular signaling cascades. We hypothesize that GRK-2 will upregulate following chronic stress to suppress chronic adrenergic receptor signaling, but that the increase may be insufficient to prevent the onset of anxiety and impulse control that are regulated by the BNST and PFC. Female rats were exposed to a chronic mild stress paradigm that consisted of being exposed to various stressors during the day and night for a total of 4 days. The BNST and PFC were extracted through laser capture microscopy from control and stressed rats, then GRK-2 gene expression in the targeted tissue was measured by rtPCR. GRK-2 mRNA showed a significant increase in chronically stressed rats compared to control animals in the BNST. Data for the PFC is currently being collected. Future studies will investigate whether manipulating GRK-2 expression can make an organism more or less susceptible to stress-induced behavioral changes.
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