Correlation Study On Expression Of CaMKⅡ And ERK In Cerebral Cortex Of Autism Mouse Model

Objective To probe the function of CaMKII and ERK in the mechanism of autism spectrum disorders.Methods Female Wistar rats gained a single intraperitoneal administration of sodium valproate(VPA,600 mg/kg)at 12.5 d after pregnancy,whose offsprings were the model group;while the other pregnancy rats gained the same dose normal saline,whose offsprings were the control group.Both groups were observed by the HE staining,western blot and immunohistochemistry of CaMKII and ERK,and image analysis 1 d,7 d,14 d,28 d,56 d after birth.Results The rats in the experimental group showed developmental retardation,low body weight,delayed eye opening,poor coordination of swimming,abnormal orientation reaction and so on.In the experimental group,the behavior of the young rats was characterized by the reduction of social behavior,the repetition of the stereotyped behavior,the social orientation and the social communication.HE staining indicated that the amount of cortical neurons reduced on 1 d and 7 d after birth in the model group,rapidly increased on 14 d after birth,and then maintained in high level.For western blot and immunohistochemistry,the integrated optical density(IOD)of CaMKII and ERK increased in cortex on 1~14 d after birth(P<0.001)in both groups,were no difference on 21 d,and were stable 28 d after birth(P>0.05).Compared with the control group,the IOD of CaMKII and ERK increased much more at every time point(P<0.001)in the model group.CaMKII and ERK was was increased on 1d,7d(P<0.001),significantly increased on 14d(P<0.001),and increased to less than 28 d after birth(P>0.05).Conclusions The expression of CaMKII and ERK of cerebral cortex neurons increases in the autism spectrum disorders model rats;the expression of CaMKII and ERK of cerebral cortex neurons is consistent in time;the neurons of autism spectrum disorders model rats exist excessive expression and even stagnation.