Mechanisms for gravity stress-induced synaptic plasticity in rat hippocampus

重力应激诱导大鼠海马突触可塑性的机制

基本信息

批准号：
16591853
负责人：
KUMEI Yasuhiro
金额：
$ 2.05万
依托单位：
Tokyo Medical and Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-16591853/
关键词：
hippocampus gravity synaptic plasticity LTP telemetry パッチクランプ脳スライス

项目摘要

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.

我们测量了CA1区域中的场电位，以应对Schaffer侧支的电刺激。在100 vs. 1Hz刺激之间，负挠度的振幅相对比率在2G分段中增加了40％。高点增强了CA1区域的单位活动和突触传播，这可能是大鼠重力反应机理的基础。振幅的相对比在1g（基础水平）时为1.3，在2G超级强度时增加到1.8。海马CA1区域突触传播的效率通过2G暴露提高。高度诱导的早期LTP（长期增强）可能反映了CA1区域的发射频率的增加。 Ishii等人报告了类似的数据。在该早期期间，LTP在暴露于4G的小鼠中诱导了48小时，并增强了AMPA受体磷酸化。另一组报告了海马LTP诱导的急性行为应力的时间依赖性调节。数据表明，海马LTP，谷氨酸 - 受体，Ca ^<2+>，5-羟色胺（5-HT）LTP的实施和GABA抑制性神经元在海马可塑性上的分子机制，最终导致无序的学习和记忆力。海马，杏仁核和下丘脑是通过神经元回路相互联系的。这些区域中神经元活性的调节可能在对重力改变反应的基础机制中起着致病作用。