1·The abnormal metabolism and excess release of Glutamic acid as well as high-frequency stimulation to the postsynaptic receptor induce excitatory neural toxicity, resulting in the death of neurons.
因谷氨酸代谢异常，过度释放和对突触后受体的高频刺激，引起了兴奋性神经毒性，导致神经元死亡。
2·Postsynaptic potentials manifested current effect and frequency dependency and their IPSP displayed a prolonged inhibition.
突触后电位表现电流效应和频率依赖性，其IPSP具有长时程的抑制作用。
3·These results indicate that the mutation does not interfere with the ability of agrin to induce postsynaptic structures but that it dramatically perturbs the maintenance of the neuromuscular junction.
这些结果表明，该突变不仅影响集聚蛋白诱导突触后结构的功能，也影响神经肌肉接头功能的维持。
4·The previous studies indicated it produced anesthetic effect through its mimic GABA action, which enhanced central inhibition mediated by postsynaptic GABAa receptors.
以往研究认为其具有拟gaba样作用，通过增强突触后gaba_a受体介导的中枢抑制而产生麻醉作用。
5·At the holding potential of 0 mV, spontaneous inhibitory postsynaptic currents (IPSCs) and dorsal root stimulation-evoked IPSCs were recorded as outward currents.
在钳制电压为0毫伏条件下，记录自发的和背根刺激引起的抑制性突触后电流。