Effects of congenital HCMV infection on synaptic plasticity in dentate gyrus (DG) of rat hippocampus.

This study was carried out to investigate whether the congenital HCMV infection affect the induction and maintenance of LTP /DP. Rat models of Sprague-Dawley rats congenitally infected by HCMV were made. Field excitatory postsynaptic potentials (EPSPs) were recorded in the hippocampal slices of offspring rats (50-65days) to study alterations of LTP /DP in area dentate gyrus (DG) of the hippocampus after congenital infection. The Ca(2+) and mRNA level of calmodulin (CaM) in the hippocampus neurons of the experiment group (congenital infected by HCMV) and the control group were measured;The input/output (I/O) curves of the EPSP slope PS amplitude in area DG in experiment group were significantly depressed when compared to control group (P<0.05). LTP of the EPSP slope and PS amplitude in area DG of the hippocampus was 137±4% (EPSP) and 225±11% (PS) in control rats and 115±9% (EPSP) and 163±7% (PS) in experiment rats (EPSP: F=25.29,P<0.05;PS: F=74.33 P<0.05, two-way ANOVA with Tukey test); DP of the EPSP slope and PS amplitude was 86±3% (EPSP) and 85±2% (PS) in control rats and 94±5% (EPSP) and 93±4% (PS) in congenitally infected rats (EPSP: F=5.62, P<0.05;PS: F=4.22, P<0.05, two-way ANOVA with Tukey test) . At the same time, intracellular [Ca(2+)] and mRNA level of CaM in the hippocampus neurons of the experiment group were significantly increased than that of in the controls ([Ca(2+)]: P<0.01;CaM mRNA: P<0.01) . The results demonstrate that congenital HCMV infection could reduce the range of synaptic plasticity in the Sprague-Dawley rats, which may trigger the dysfunction of learning and memory through disrupting the calcium balance.