Aberrant amygdala-dependent fear memory in corticosterone-treated mice

Publication date: Available online 16 August 2018Source: NeuroscienceAuthor(s): Ryo Inagaki, Shigeki Moriguchi, Kohji FukunagaAbstractAnxiety disorder is a major psychiatric disorder characterized by fear, worry, and excessive rumination. However, the molecular mechanisms underlying neural plasticity and anxiety remain unclear. Here, we utilized a mouse model of anxiety-like behaviors induced by the chronic administration of corticosterone (CORT) to determine the exact mechanism of each region of the fear circuits in the anxiety disorders. Chronic CORT treated mice showed significant increase in anxiety-related behaviors as assessed by the elevated plus maze, light-dark, open-field, and marble-burying tasks. In addition, chronic CORT treated mice exhibited abnormal amygdala-dependent tone-induced fear memory but normal hippocampus-dependent contextual memory. Consistent with amygdala hyperactivation, chronic CORT treated mice showed significantly increased numbers of c-Fos-positive cells in the basolateral amygdala (BLA) after tone stimulation. Long-term potentiation (LTP) was markedly enhanced in the BLA of chronic CORT treated mice compared to that of vehicle-treated mice. Immunoblot analyses revealed that autophosphorylation of Ca2+/calmodulin-dependent protein kinase (CaMK) IIα at threonine 286 and phosphorylation of cyclic-adenosine-monophosphate -response-element-binding protein (CREB) at serine 133 were markedly increased in the BLA of chronic CORT treated mice after ...

Source: Neuroscience - August 16, 2018 Category: Neuroscience Source Type: research