Although melamine exposure induces cognitive deficits and dysfunctional neurotransmission in hippocampal Cornus Ammonis (CA) 1 region of rats, it is unclear whether the neural function, such as neural oscillations between hippocampal CA3–CA1 pathway and postsynaptic receptors involves in these effects. The levels of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) subunit glutamate receptor (GluR) 1 and GluR2/3 in CA1 region of melamine-treated rats, which were intragastric treated with 300 mg/kg/day for 4 weeks, were detected. Following systemic or intra-hippocampal CA1 injection with GluR2/3 agonist, spatial learning of melamine-treated rats was assessed in Morris water maze (MWM) task. Local field potentials were recorded in CA3–CA1 pathway before and during behavioral test. General Partial Directed Coherence approach was applied to determine directionality of neural information flow between CA3 and CA1 regions. Results showed that melamine exposure reduced GluR2/3 but not GluR1 level and systemic or intra-hippocampal CA1 injection with GluR2/3 agonist effectively mitigated the learning deficits. Phase synchronization between CA3 and CA1 regions were significantly diminished in delta, theta and alpha oscillations. Coupling directional index and strength of CA3 driving CA1 were marked reduced as well. Intra-hippocampal CA1 infusion with GluR2/3 agonist significantly enhanced the phase locked value and reversed the melamine-induced reduction in the neural information flow (NIF) from CA3 to CA1 region. These findings support that melamine exposure decrease the expression of GluR2/3 subunit involved in weakening directionality index of NIF, and thereby induced spatial learning deficits.

虽然三聚氰胺暴露会导致大鼠海马角部 (CA) 1 区域的认知缺陷和神经传递功能障碍，但尚不清楚海马 CA3-CA1 通路与突触后受体之间的神经振荡等神经功能是否参与这些影响。三聚氰胺治疗大鼠CA1区α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（AMPAR）亚基谷氨酸受体（GluR）1和GluR2/3水平，300 mg/kg/天，持续 4 周，均被检测到。在全身或海马内 CA1 注射 GluR2/3 激动剂后，在莫里斯水迷宫 (MWM) 任务中评估了三聚氰胺治疗大鼠的空间学习。在行为测试之前和期间在 CA3-CA1 通路中记录局部场电位。应用一般部分定向相干方法来确定 CA3 和 CA1 区域之间神经信息流的方向性。结果表明，三聚氰胺暴露降低了 GluR2/3 而不是 GluR1 水平，全身或海马内 CA1 注射 GluR2/3 激动剂有效地减轻了学习缺陷。CA3 和 CA1 区域之间的相位同步在 delta、theta 和 alpha 振荡中显着减弱。CA3驱动CA1的耦合方向指数和强度也显着降低。海马内 CA1 与 GluR2/3 激动剂输注显着增强了锁相值并逆转了三聚氰胺诱导的从 CA3 到 CA1 区域的神经信息流 (NIF) 减少。