Dysfunction of calcium/calmodulin/CaM kinase IIα cascades in the medial             prefrontal cortex in post-traumatic stress disorder.
Post-traumatic stress disorder (PTSD) is a significant problem that may             affect individuals who have been exposed to a traumatic event or events, including             combat, violent crime or childhood abuse. The medial prefrontal cortex (mPFC)             is known to be significantly involved in emotional adjustment, particularly introspection,             amygdala inhibition and emotional memory. In the acute phase of severe traumatic             stress, the mPFC appears to undergo a change in plasticity for a short time, which             suggests that the mPFC may be the reponse-sensitizing region. Calcium (Ca2+) is             one of most significant intracellular messengers; the appropriate concentration             of Ca2+ is necessary for neuronal excitability. When the Ca2+ concentration increases,             Ca2+, calmodulin (CaM) and CaM kinase IIα (CaMKIIα) combine together to form the             Ca2+‑CaM‑CaMKIIα signaling pathway, which is important in the plasticity of the             central nervous system, learning and memory, mind, behavior and other types of             cognitive activities. Our team studied the changes in the Ca2+-CaM-CaMKIIα levels             in the mPFC of rats following a single-prolonged stress (SPS). The SPS, a credible             method for establishing a rat model of PTSD, has been internationally recognized.             The free intracellular Ca2+ concentration in the mPFC in the PTSD group was significantly             higher than that in the control group 1 day after SPS exposure (P<0.05) and             decreased 7 days after SPS; CaM expression significantly increased, while CaMKIIα             expression significantly decreased in the mPFC 1 day after SPS compared with the             control group. These findings suggest dysfunction of the Ca2+-CaM-CaMKIIα cascades             in the mPFC, which may relate to the pathogenesis of the abnormal functioning             of the mPFC in PTSD.
Department of Histology and Embryology, Institute of Pathology and Pathophysiology, Basic Medical Sciences College, China Medical University, and Department of Orthopaedic Surgery, Shengjing Hospital, Shenyang, Liaoning 110001, PR China.
Yu
Y
Wen
Bin
B
Li
Fang
F
Han
Enhua
E
Wang
Yuxiu
Y
Shi
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000235:genetics / Q000378:metabolism*; D002147:Calmodulin / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D008297:Male; D017397:Prefrontal Cortex / Q000166:cytology / Q000201:enzymology* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction; D013313:Stress Disorders, Post-Traumatic / Q000473:pathology
D002147:Calmodulin; D012333:RNA, Messenger; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D002118:Calcium