Prenatal melamine exposure induces impairments of spatial cognition and hippocampal synaptic plasticity in female adolescent rats

- Prenatal melamine exposure (PME) induces cognitive defects in female offspring.
- PME depresses depotentiation, but not LTP, in hippocampal CA1 area.
- PME impairs synaptic function, such as PTP and PPR.
- Synaptic plasticity imbalance may be contributed to the cognitive deficits.

Developmental exposure to melamine induces long-term effects on brain and behavior in male rodents. To examine whether this prenatal event damages cognitive function in female offspring, we evaluated the behavioral effects and further attempted to investigate synaptic function. Prenatal melamine exposure (PME) was given by oral treatment to pregnant females through the whole gestational days with 400 mg/day/kg bodyweight. On postnatal day (PD) 36, female offspring were assessed for spatial cognition in the Morris Water Maze (MWM) test. Simultaneously, the alterations in hippocampal synaptic plasticity in Schaffer collaterals-CA1 pathway in vivo were measured. The results of behavioral test showed that PME lead serious deficits of memory and re-acquisition abilities. PME depressed depotentiation in the hippocampal CA1 area of the PME group, but no alteration in LTP. Furthermore, variations of post-tetanic potentiation (PTP) and paired-pulse facilitation (PPF) were also observed in this pathway. This finding indicated that the PME affected spatial cognition in adolescent females, and the impairment of hippocampal synaptic functions may partly play a significant role in these effects.