Mechanisms for gravity stress-induced synaptic plasticity in rat hippocampus

我们测量了当电刺激Schaffer‘s侧支时，CA1区的场势。在2G脑片中，100 Hz刺激与1 Hz刺激相比，负偏转幅度的相对比率增加了40%。超重增强了CA1区的单位活动和突触传递，这可能是大鼠重力反应机制的基础。波幅相对比值在1G(基础水平)时为1.3，在2G超重时增加到1.8。2G暴露可提高大鼠海马CA1区突触传递的效率。超重力诱发的早期LTP可能反映了CA1区放电频率的增加。石井等人也报告了类似的数据。在这一早期阶段，4G暴露48小时的小鼠诱导了LTP，AMPA受体的磷酸化增强。另一组报告了急性行为应激对海马LTP诱导的位置和时间依赖的调节。数据表明，海马区LTP、谷氨酸受体、Ca~(2+)和Gt~(2+)、LTP的5-羟色胺(5-HT)强化和GABA抑制神经元对海马可塑性的分子机制，最终将导致对重力信息的学习和记忆障碍。海马体、杏仁核和下丘脑是由神经元回路相互连接的结构。这些区域神经元活动的调节可能在对重力变化的反应机制中起到致病作用。

We measured the field potential in the CA1 region as responding to electrical stimulation of Schaffer's collaterals. The relative ratio of amplitude of the negative deflection, as compared between 100 vs. 1Hz stimulation, was 40% increased in the 2G-slices. Hypergravity enhanced unit activities and synaptic transmission in the CA1 region, which may underlie the gravity-response mechanism of rat. The relative ratio of amplitude was 1.3 at 1G (basal level), and increased to 1.8 at 2G hypergravity. The efficiency of synaptic transmission in the hippocampal CA1 region was increased by 2G-exposure. The hypergravity-induced early-phase LTP (long-term potentiation) might reflect the increase of firing frequency in the CA1 region. Similar data were reported by Ishii et al. in that early-phase LTP was induced in mice that were exposed to 4G for 48 hrs with enhancement of AMPA receptor phosphorylation. Another group reported the site and time-dependent modulation of acute behavioral stress on hippocampal LTP induction. Data suggest molecular mechanism for the hippocampal LTP, glutamate-receptor, Ca ^<2+>, serotonin (5-HT) enforcement of LTP, and GABA inhibitory neurons on hippocampal plasticity, which will finally result in disordered learning and memory of gravitational informations. Hippocampus, amygdala, and hypothalamus are interconnected structures by neuronal circuit. The modulation of neuronal activity in these areas might play causative roles in the mechanism underlying the response to gravitational alteration.