The Effect Of Overexpressed ?CaMK?-F89G On Stress-induced Anxiety-like And Depression-like Behavior

Post-traumatic stress disorder?PTSD?is a symptom that could develop following exposure to traumatic events.Comorbidities include substance abuse,depression and anxiety.Studies have been demonstrated that PTSD may be related to signal pathways involving Ca²⁺,CaM as well as aCaMK?.However,it is still not clear that what role does aCaMKII take in PTSD and whether memory reconsolidation can be applied into the treatment of PTSD.The current studies aim to investigate the role of CaMKII in PTSD formation using aCaMK?-F89G transgenic mice.By adopting the restraint method to generate PTSD mice model,we were able to compare behavioral phenotype of transgenic mice with their wild-type littermates.We found that both transgenic and wild-type mice showed PTSD syndrome,including depression-like and anxiety-like behavior,upon 24-hour restrain treatment.PTSD syndrome lasted for at least 4 weeks both in aCaMK?-F89G transgenic and wide-type mice.Our study demonstrates that forebrain overexpression of aCaMK? has no effect on PTSD formation.Further we attempted to alleviate the PTSD syndrome by disruption of memory reconsolidation process to erase the traumatic memory.By up regulating the expression of aCaMK?-F89G in forebrain after memory reactivation,we have shown that fear memory could be erased.However,both the depression-like and anxiety-like behavioral phenotype still remain upon the same manipulation.Overall,our studies provide preliminary studies to understand the roles of aCaMKII-F89G in PTSD.