Comparison Impairments of Spatial Cognition and Hippocampal Synaptic Plasticity Between Prenatal and Postnatal Melamine Exposure in Male Adult Rats.

Our previous investigation showed that melamine in offspring hippocampus appeared to not be the critical factor for cognitive defects. The present study was to investigate whether the cognitive impairments induced by prenatal and postnatal melamine exposure and persisted into adulthood, and to evaluate the differences of the exposures in affecting hippocampus-depended cognition and synaptic plasticity. Wistar rats were exposed to melamine through the whole gestational period or from postnatal day (PD) 21 to PD41, and then tested on PD90. The experiments of water maze and hippocampal synaptic plasticity in vivo were performed to assess the effects on spatial cognition and synaptic impairments. The results indicated that cognitive defects were induced by exposures to either prenatal or postnatal melamine, whereas there was a more serious damage in prenatal. Histological evidence further showed that there were the detrimental effects of both prenatal and postnatal effects. Paired-pulse facilitation ratio and post-tetanic potentiation were severely impacted in prenatal-exposed rats but not postnatal-exposed ones. Both exposures to prenatal and postnatal melamine impaired long-term potentiation, while there was severe damage to prenatal animals. These data suggest that the detrimental effects of prenatal and postnatal melamine on cognition and hippocampal synaptic plasticity could persist into adulthood, and the impairment of prenatal exposure was to some extent more severe. Hence, prenatal and postnatal exposures to melamine may have different effects on hippocampus-dependent learning and memory, which would most likely result from differentially adversely properties on the hippocampal CA1 synaptic function.