Imbalanced synaptic plasticity induced spatial cognition impairment in male offspring rats treated with chronic prenatal ethanol exposure.

BACKGROUND As chronic prenatal ethanol (EtOH) exposure (CPEE) may cause deficiencies in a variety of behavioral and cognitive functions, the aim of present study is to investigate the effects of CPEE on spatial learning and memory and examine the action of CPEE on synaptic plasticity balance in the hippocampus of adolescent male rats. METHODS The animal model was produced by EtOH exposure throughout gestational period with 4 g/kg bodyweight, while the male offspring rats were used in the study. Morris water maze (MWM) test was performed, and then, long-term potentiation (LTP) and depotentiation were recorded from Schaffer collaterals to CA1 region in the hippocampus. RESULTS It was shown that escape latencies in learning period and re-acquisition period were prolonged in CPEE-treated group compared with that in control group. Furthermore, LTP was drastically inhibited, and depotentiation was distinctly enhanced in CPEE-treated group compared with that in control group. CONCLUSIONS It is suggested that the balance between cognitive stability and flexibility was broken by the bidirectional effects of long-term synaptic plasticity. In addition, the spatial cognition was attenuated by the alteration of synaptic plasticity balance in CPEE-treated male adolescent rats.