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Dysfunction of Ca2+/ CaM kinase IIA cascades in basolateral amygdala of posttraumatic stress disorder rats

Published online by Cambridge University Press:  16 April 2020

Y. Shi
Affiliation:
China Medical University, Shenyang, China
F. Han
Affiliation:
China Medical University, Shenyang, China

Abstract

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Objective

To explore changes of Ca2+-CaM-CaMKIIα in basolateral amygdala of PTSD rats may reveal part of the pathogensis.

Methods

The SPS-method was used to set up the rat PTSD models. A total of 90 male Wistar rats were randomly divided into1d, 4d, 7d, 14d groups of SPS and normal control groups. The intracellular free calcium level in basolateral amygdala was examined by fluorescence spectrophotometer. CaM and CaMKIIα expression in basolateral amygdala were examined by immunohistochemistry, western blotting and reverse transcription-polymerase chain reaction (RT-PCR).

Results

The intracellular free calcium level reached the peak 1 day after SPS stimulation, then gradually decreased to normal level. The expression of CaM 1day after SPS is also the most and then decreased to normal level. In contrast, CaMKIIα expression showed a significant down-regulation 1day after SPS throughout and then gradually increased to normal level. This findings suggest dysfunction of Ca2+-CaM-CaMKIIα in basolateral amygdala of PTSD rats.

Conclusion

Thus, the trauma-induced enhanced anxiety appear to be associated with, and possibly caused by, changes of Ca2+-CaM-CaMKIIα in basolateral amygdala.

Type
P01-178
Copyright
Copyright © European Psychiatric Association 2011
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