Enhancement of the function of aged synapses and its mechanism

我们在我们先前的研究中发现了一个关于老年大脑的hypofunction是由decreased synaptic transmission引起的，而那个被decreased的Ca-D12 +-D1 influx通过voltage-dependent calcium channel引起的。基于这些发现，我们瞄准了在这个研究中增强老年大脑的协同传输。（1） Gangliosides enriched on synaptic Management branes were examined for their effManagement on CaイイD12+イエD1influx。恒河苷、GM 1或GQ 1b，从合成酶组中增加了诱导的乙酰胆碱素释放。这一影响被证明是为了增强钙通道的有效性。（2）长期潜力作为协同可塑性的标志物，通过恒河苷GM 1或GQ 1b得到增强。（3）在尝试应用恒河素对人类案例、sialyl化合物、恒河素模拟，以及较小的分子重量被专门用于对自然恒河素的高级作用。Sialyl Cholesterol被发现用于增强synaptic transmission

We have found in our previous studies that the hypofunction of the aged brain is caused by decreased synaptic transmission, and that the diminished transmission is due to decreased CaィイD12+ィエD1influx through voltage-dependent calcium channels. Based on these findings, we aimed to enhance the synaptic transmission of the aged brain in this study. (1) Gangliosides enriched on synaptic membranes were examined for their effects on CaィイD12+ィエD1influx. Ganglioside, GM1 or GQ1b, increased the depolarization-induced acetylcholine release from synaptosomes. This effect was proved to be due to enhanced efficacy of calcium channels. (2) Long-term potentiation as a marker of synaptic plasticity was enhanced by ganglioside GM1 or GQ1b. (3) In the attempt to apply the ganglioside effects on human cases, sialyl compounds, ganglioside analognes, of smaller molecular weight were speculated to be superior to natural gangliosides. Sialyl cholesterol was found to enhance the synaptic transmission.