Dysfunction of Ca2+/CaM kinase IIα cascades in the amygdala in post-traumatic stress disorder

Abstract

Single-prolonged stress (SPS) is an established animal model for post-traumatic stress disorder (PTSD). The calcium (Ca2+)-calmodulin (CaM)-CaM kinase (K)IIα signal passage plays an important role in the plasticity of central nervous, learning and memory, mind and behavior and other types of cognitive activities. The amygdala is known to play an important role in fear, rage and emotional memory. In this study, we investigated changes in Ca2+-CaM-CaMKIIα in the basolateral amygdala of rats after SPS which may reveal part of the pathogenesis of PTSD. The intracellular free calcium level in the basolateral amygdala was examined by fluorescence spectrophotometry. CaM and CaMKIIα expression in basolateral amygdala was examined using immunohistochemistry, western blotting and reverse transcription-polymerase chain reaction. The intracellular free calcium level in the basolateral amygdala was increased when compared to that in the control group 1 day after SPS exposure (P<0.05). CaM expression significantly increased, and CaMKIIα expression significantly decreased (P<0.05) in the basolateral amygdala after SPS. These findings suggest dysfunction of Ca2+-CaM-CaMKIIα in the basolateral amygdala of SPS rats, which may play important roles in the pathogenesis of PTSD rats.